Downregulation of LncRNAH19 and MiR-675 Promotes Migration and Invasion of Human Hepatocellular Carcinoma Cells through AKT/GSK-3β/Cdc25A Signaling Pathway
Summary: LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for miR-675. However, it is unknown whether LncRNAH19 and miR-675 are involved in the migration and invasion of hepatocellular carcinoma (HCC) c...
Saved in:
Published in | Journal of Huazhong University of Science and Technology. Medical sciences Vol. 34; no. 3; pp. 363 - 369 |
---|---|
Main Author | |
Format | Journal Article |
Language | English |
Published |
Heidelberg
Huazhong University of Science and Technology
01.06.2014
Department of Hepatobiliary Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China Department of Hepatobiliary Surgery, the Affiliated Hospital of Guilin Medical College, Guilin 541001, China%Department of Hepatobiliary Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China%Department of Surgical Laboratory, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China |
Subjects | |
Online Access | Get full text |
ISSN | 1672-0733 1993-1352 |
DOI | 10.1007/s11596-014-1284-2 |
Cover
Loading…
Abstract | Summary: LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for miR-675. However, it is unknown whether LncRNAH19 and miR-675 are involved in the migration and invasion of hepatocellular carcinoma (HCC) cells. The purpose of this study was to investigate the effect and mechanism of LncRNAH19 and miR-675 on migration and invasion of HCC cells. The migration and invasion of HCC cells were measured by Transwell migration and invasion assays after transfection of HCC cells with miR-675 inhibitors and LncRNAH19siRNA. The levels of LncRNAH19 and miR-675 were detected by quantitative reverse transcriptase real-time polymerase chain reaction (qRT-PCR), and the protein expression of AKT, GSK-3[3 and Cdc25A by Western blotting analysis. The expression levels of LncRNAHI9 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the migration of HCC cells (P〈0.01) as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the invasion of HCC cells (P〈0.01) as compared with the control group. Western blotting analy- sis showed that the expression levels of AKT and Cdc25A were significantly increased (P〈0.05), and the expression level of GSK-313 was significantly decreased (P〈0.05) after treatment with miR-675 inhibitors and LncRNAH19siRNA as compared with the control group. These findings suggested that inhibition of LncRNAH 19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3[3/Cdc25A signaling pathway. |
---|---|
AbstractList | LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for miR-675. However, it is unknown whether LncRNAH19 and miR-675 are involved in the migration and invasion of hepatocellular carcinoma (HCC) cells. The purpose of this study was to investigate the effect and mechanism of LncRNAH19 and miR-675 on migration and invasion of HCC cells. The migration and invasion of HCC cells were measured by Transwell migration and invasion assays after transfection of HCC cells with miR-675 inhibitors and LncRNAH19siRNA. The levels of LncRNAH19 and miR-675 were detected by quantitative reverse transcriptase real-time polymerase chain reaction (qRT-PCR), and the protein expression of AKT, GSK-3β and Cdc25A by Western blotting analysis. The expression levels of LncRNAH19 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the migration of HCC cells (P<0.01) as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the invasion of HCC cells (P<0.01) as compared with the control group. Western blotting analysis showed that the expression levels of AKT and Cdc25A were significantly increased (P<0.05), and the expression level of GSK-3β was significantly decreased (P<0.05) after treatment with miR-675 inhibitors and LncRNAH19siRNA as compared with the control group. These findings suggested that inhibition of LncRNAH19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3β/Cdc25A signaling pathway.LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for miR-675. However, it is unknown whether LncRNAH19 and miR-675 are involved in the migration and invasion of hepatocellular carcinoma (HCC) cells. The purpose of this study was to investigate the effect and mechanism of LncRNAH19 and miR-675 on migration and invasion of HCC cells. The migration and invasion of HCC cells were measured by Transwell migration and invasion assays after transfection of HCC cells with miR-675 inhibitors and LncRNAH19siRNA. The levels of LncRNAH19 and miR-675 were detected by quantitative reverse transcriptase real-time polymerase chain reaction (qRT-PCR), and the protein expression of AKT, GSK-3β and Cdc25A by Western blotting analysis. The expression levels of LncRNAH19 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the migration of HCC cells (P<0.01) as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the invasion of HCC cells (P<0.01) as compared with the control group. Western blotting analysis showed that the expression levels of AKT and Cdc25A were significantly increased (P<0.05), and the expression level of GSK-3β was significantly decreased (P<0.05) after treatment with miR-675 inhibitors and LncRNAH19siRNA as compared with the control group. These findings suggested that inhibition of LncRNAH19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3β/Cdc25A signaling pathway. LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for miR-675. However, it is unknown whether LncRNAH19 and miR-675 are involved in the migration and invasion of hepatocellular carcinoma (HCC) cells. The purpose of this study was to investigate the effect and mechanism of LncRNAH19 and miR-675 on migration and invasion of HCC cells. The migration and invasion of HCC cells were measured by Transwell migration and invasion assays after transfection of HCC cells with miR-675 inhibitors and LncRNAH19siRNA. The levels of LncRNAH19 and miR-675 were detected by quantitative reverse transcriptase real-time polymerase chain reaction (qRT-PCR), and the protein expression of AKT, GSK-3β and Cdc25A by Western blotting analysis. The expression levels of LncRNAH19 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the migration of HCC cells (P<0.01) as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the invasion of HCC cells (P<0.01) as compared with the control group. Western blotting analysis showed that the expression levels of AKT and Cdc25A were significantly increased (P<0.05), and the expression level of GSK-3β was significantly decreased (P<0.05) after treatment with miR-675 inhibitors and LncRNAH19siRNA as compared with the control group. These findings suggested that inhibition of LncRNAH19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3β/Cdc25A signaling pathway. Summary: LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for miR-675. However, it is unknown whether LncRNAH19 and miR-675 are involved in the migration and invasion of hepatocellular carcinoma (HCC) cells. The purpose of this study was to investigate the effect and mechanism of LncRNAH19 and miR-675 on migration and invasion of HCC cells. The migration and invasion of HCC cells were measured by Transwell migration and invasion assays after transfection of HCC cells with miR-675 inhibitors and LncRNAH19siRNA. The levels of LncRNAH19 and miR-675 were detected by quantitative reverse transcriptase real-time polymerase chain reaction (qRT-PCR), and the protein expression of AKT, GSK-3[3 and Cdc25A by Western blotting analysis. The expression levels of LncRNAHI9 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the migration of HCC cells (P〈0.01) as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the invasion of HCC cells (P〈0.01) as compared with the control group. Western blotting analy- sis showed that the expression levels of AKT and Cdc25A were significantly increased (P〈0.05), and the expression level of GSK-313 was significantly decreased (P〈0.05) after treatment with miR-675 inhibitors and LncRNAH19siRNA as compared with the control group. These findings suggested that inhibition of LncRNAH 19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3[3/Cdc25A signaling pathway. Summary LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for miR-675. However, it is unknown whether LncRNAH19 and miR-675 are involved in the migration and invasion of hepatocellular carcinoma (HCC) cells. The purpose of this study was to investigate the effect and mechanism of LncRNAH19 and miR-675 on migration and invasion of HCC cells. The migration and invasion of HCC cells were measured by Transwell migration and invasion assays after transfection of HCC cells with miR-675 inhibitors and LncRNAH19siRNA. The levels of LncRNAH19 and miR-675 were detected by quantitative reverse transcriptase real-time polymerase chain reaction (qRT-PCR), and the protein expression of AKT, GSK-3β and Cdc25A by Western blotting analysis. The expression levels of LncRNAH19 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the migration of HCC cells ( P <0.01) as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the invasion of HCC cells ( P <0.01) as compared with the control group. Western blotting analysis showed that the expression levels of AKT and Cdc25A were significantly increased ( P <0.05), and the expression level of GSK-3β was significantly decreased ( P <0.05) after treatment with miR-675 inhibitors and LncRNAH19siRNA as compared with the control group. These findings suggested that inhibition of LncRNAH19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3β/Cdc25A signaling pathway. |
Author | 吕军 马宁 陈锡林 黄晓卉 汪谦 |
AuthorAffiliation | Department of Hepatobiliary Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China Department of Surgical Laboratory, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China Department of Hepatobiliary Surgery, the Affiliated Hospital of Guilin Medical College, Guilin 541001, China |
AuthorAffiliation_xml | – name: Department of Hepatobiliary Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China;Department of Hepatobiliary Surgery, the Affiliated Hospital of Guilin Medical College, Guilin 541001, China%Department of Hepatobiliary Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China%Department of Surgical Laboratory, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China |
Author_xml | – sequence: 1 fullname: 吕军 马宁 陈锡林 黄晓卉 汪谦 |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24939300$$D View this record in MEDLINE/PubMed |
BookMark | eNp9kd1u0zAUxyM0xD7gAbhB5g4JhfojtuPLqsA6rcC0jWvrNHHSlMTu7ISu78JT8CA8Ey4pQ-JiV7bO-f3P1_80ObLOmiR5SfA7grGcBEK4EikmWUponqX0SXJClGIpYZwexb-QNMWSsePkNIQ1xlwKmj1LjmmmmGIYnyQ_3rut9aYeWugbZ5Gr0MIW15-nc6IQ2BJ9aq5TITm68q5zvQkxUPuR3acv7HcIB-F86MCiudlA7wrTtrGmRzPwRWNdB2gWQwH1K--GeoWml7eT85vLlP36OZmVBeVTdNPUFtrG1ugK-tUWds-TpxW0wbw4vGfJ148fbmfzdPHl_GI2XaRFhkWfViCVKEEVZFkSXHKOc5KbTLAKhKCQKSyNKBmvFK5yIJkwucG5lDJjuarKgp0lb8e6W7AV2Fqv3eDjKEH369238v5-qQ2NV8YMExLpNyO98e5uMKHXXRP2-4I1bgiacCa5ogLv0VcHdFh2ptQb33Tgd_rv_SNARqDwLgRvqgeEYL33WI8e69hd7z3WNGrkf5qi6f840nto2keVdFSG2MXWxv9b9DHR60O7lbP1XdQ9zJgpxUXOOPsNxnbEwg |
CitedBy_id | crossref_primary_10_3390_ncrna6030034 crossref_primary_10_12998_wjcc_v9_i32_9699 crossref_primary_10_1016_j_mrrev_2021_108375 crossref_primary_10_1139_bcb_2019_0362 crossref_primary_10_1016_j_ijdevneu_2018_03_009 crossref_primary_10_1016_j_chemosphere_2018_05_048 crossref_primary_10_1007_s12010_022_04191_1 crossref_primary_10_1002_jcb_26883 crossref_primary_10_1155_2017_6049480 crossref_primary_10_3934_molsci_2016_2_104 crossref_primary_10_1093_bfgp_elw011 crossref_primary_10_1007_s12072_024_10722_1 crossref_primary_10_1155_2015_473942 crossref_primary_10_1155_2019_6587429 crossref_primary_10_1177_10732748241284821 crossref_primary_10_1155_2018_8126208 crossref_primary_10_3389_fmed_2024_1456963 crossref_primary_10_3389_fcell_2021_796740 crossref_primary_10_1016_j_phrs_2020_105195 crossref_primary_10_3390_ncrna9020019 crossref_primary_10_3748_wjg_v24_i5_549 crossref_primary_10_1080_21655979_2021_1995573 crossref_primary_10_1016_j_mrrev_2015_08_002 crossref_primary_10_4236_jct_2018_93026 crossref_primary_10_1042_BSR20160532 crossref_primary_10_1007_s11596_015_1452_z crossref_primary_10_1002_jcb_29649 crossref_primary_10_1007_s13402_018_0412_6 crossref_primary_10_3727_096504015X14496932933575 crossref_primary_10_3727_096504016X14549667334007 crossref_primary_10_1016_j_gene_2017_12_051 crossref_primary_10_1007_s11596_024_2899_6 crossref_primary_10_1016_j_genrep_2022_101724 crossref_primary_10_1159_000495151 crossref_primary_10_1007_s13577_023_00958_8 crossref_primary_10_3390_ijms19030682 crossref_primary_10_1155_2018_1808370 crossref_primary_10_1155_2020_1634252 crossref_primary_10_1177_1179299X17737301 crossref_primary_10_1007_s13277_016_4852_1 crossref_primary_10_1016_j_lfs_2020_118560 crossref_primary_10_18632_aging_205523 crossref_primary_10_1155_2018_1690747 crossref_primary_10_1186_s12885_018_4831_6 crossref_primary_10_1002_jcp_27269 crossref_primary_10_3748_wjg_v23_i32_5860 crossref_primary_10_1186_s12943_015_0452_8 crossref_primary_10_2217_epi_2021_0165 crossref_primary_10_4254_wjh_v7_i28_2781 crossref_primary_10_1186_s12943_016_0545_z crossref_primary_10_3892_mmr_2017_8264 crossref_primary_10_1007_s12038_020_00118_2 crossref_primary_10_1586_17474124_2016_1116382 crossref_primary_10_1080_15476286_2024_2440678 crossref_primary_10_3892_or_2016_4929 crossref_primary_10_1016_j_semcancer_2017_12_010 crossref_primary_10_1038_srep20559 crossref_primary_10_3892_mmr_2018_8746 crossref_primary_10_1002_jcb_26835 crossref_primary_10_1007_s11033_020_05695_x |
Cites_doi | 10.1016/j.ccr.2007.12.002 10.1371/journal.pone.0000845 10.1002/ijc.25516 10.1002/mc.10075 10.1038/nature02369 10.1261/rna.351707 10.1038/nrc1840 10.1111/febs.12185 10.1038/365764a0 10.1074/jbc.M112.342113 10.1371/journal.pgen.1003368 10.1093/carcin/bgp181 10.1038/35096075 10.1007/s12032-011-0004-z 10.1016/S0960-9822(02)00843-6 10.1093/embo-reports/kvd018 10.1016/j.gene.2012.01.012 10.1177/147323001103900608 10.1016/j.ygeno.2008.01.007 10.1158/1078-0432.CCR-09-1840 10.1371/journal.pone.0044206 10.1038/sj.bjc.6606010 10.1093/hmg/ddq353 10.1038/351153a0 10.1073/pnas.98.2.591 10.1016/j.canlet.2013.01.033 10.1016/j.ccr.2005.01.009 10.1016/j.chembiol.2004.07.007 10.1093/carcin/bgs381 10.1038/378785a0 10.1128/MCB.19.9.6183 10.1002/hep.23443 |
ContentType | Journal Article |
Copyright | Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2014 Copyright © Wanfang Data Co. Ltd. All Rights Reserved. |
Copyright_xml | – notice: Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2014 – notice: Copyright © Wanfang Data Co. Ltd. All Rights Reserved. |
DBID | 2RA 92L CQIGP W91 ~WA AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 2B. 4A8 92I 93N PSX TCJ |
DOI | 10.1007/s11596-014-1284-2 |
DatabaseName | 维普期刊资源整合服务平台 中文科技期刊数据库-CALIS站点 维普中文期刊数据库 中文科技期刊数据库-医药卫生 中文科技期刊数据库- 镜像站点 CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic Wanfang Data Journals - Hong Kong WANFANG Data Centre Wanfang Data Journals 万方数据期刊 - 香港版 China Online Journals (COJ) China Online Journals (COJ) |
DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
DatabaseTitleList | MEDLINE - Academic MEDLINE |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine |
DocumentTitleAlternate | Downregulation of LncRNAH19 and MiR-675 Promotes Migration and Invasion of Human Hepatocellular Carcinoma Cells through AKT/GSK-3β/Cdc25A Signaling Pathway |
EISSN | 1993-1352 |
EndPage | 369 |
ExternalDocumentID | tjykdxxb_e201403011 24939300 10_1007_s11596_014_1284_2 49956835 |
Genre | Research Support, Non-U.S. Gov't Journal Article |
GrantInformation_xml | – fundername: grants from the National Natural Science Foundation of China; Natural Science Foundation of Guangdong Province,China; Science and Technology Planning Project of Guangdong Province,China; the Foundation of the Health Department of Guangxi Province,China; the Foundation of Scientific Research and Technology Development Project of Guilin,China; the Foundation of Scientific Research and Technology Development Project of Guangxi Province,China; Foundation for Youth Teacher by Sun Yat-Sen University funderid: (.81071871,81101862 and 81172079); (.S2013010016831,and 10451008901006014); (2009B030801014,2010B060500007 and 2011B060300012); (Z2007212); (key scientific and technological projects and trial production of new products,20110321); (GuiKeGong1355005-3-5); (11ykpy16) |
GroupedDBID | -5E -5G -BR -Y2 -~C .86 .VR 06C 06D 0R~ 0VY 1N0 29K 29~ 2B. 2C~ 2J2 2KG 2KM 2LR 2RA 2~H 30V 4.4 408 40D 40E 53G 5GY 5VS 6NX 8TC 8UJ 92F 92I 92L 95- 95. 95~ 96X AAAVM AABHQ AAJKR AANXM AARHV AARTL AAYIU AAYQN AAYTO ABFTV ABJNI ABJOX ABKCH ABMNI ABNWP ABQBU ABTMW ACGFS ACHXU ACKNC ACOMO ACSNA ACUDM ADHIR ADINQ ADKPE ADURQ ADYFF ADZKW AEBTG AEGNC AEJHL AEKMD AEOHA AEPYU AETLH AEXYK AFWTZ AFZKB AGAYW AGDGC AGQMX AGWIL AGWZB AGYKE AHAVH AHBYD AHKAY AHYZX AIIXL AJBLW AJRNO ALMA_UNASSIGNED_HOLDINGS ALWAN AMKLP ARMRJ AZFZN B-. BA0 BGNMA CAG CCEZO CHBEP CIEJG COF CQIGP CS3 CSCUP CW9 D-I DPUIP EBS EJD ESBYG FA0 FEDTE FNLPD FRRFC FWDCC G-Y G-Z GGCAI GGRSB GJIRD GQ6 GQ7 HF~ HG6 HMJXF HRMNR HVGLF HZ~ IJ- IXD I~X I~Z J-C JBSCW JUIAU KOV M4Y MA- N2Q NDZJH NQJWS NU0 O9- O93 O9I O9J P9S PF0 QOR QOS R-E R89 R9I RIG ROL RPX RSV S.. S16 S1Z S27 S37 S3B SAP SCL SDH SHX SMD SNE SNX SOJ SPISZ SZ9 SZN T13 TCJ TSG TT1 TUC U2A U9L UG4 VC2 W48 W91 WK8 Z7U Z82 Z8V ZOVNA ~A9 ~WA ABQSL H13 AAYXX ADHKG AGQPQ CITATION CGR CUY CVF ECM EIF NPM 7X8 4A8 93N PSX |
ID | FETCH-LOGICAL-c406t-fa796da9c1bd10d550818e463fa662a4907e6d35f90f8a146e8e087774389fdc3 |
IEDL.DBID | U2A |
ISSN | 1672-0733 |
IngestDate | Thu May 29 04:06:47 EDT 2025 Fri Jul 11 05:39:39 EDT 2025 Thu Jan 02 23:11:23 EST 2025 Wed Aug 20 07:41:09 EDT 2025 Thu Apr 24 23:02:40 EDT 2025 Fri Feb 21 02:37:18 EST 2025 Wed Feb 14 10:36:43 EST 2024 |
IsPeerReviewed | false |
IsScholarly | false |
Issue | 3 |
Keywords | migration miR-675 invasion LncRNAH19 hepatocellular carcinoma AKT/GSK-3β/Cdc25A signaling pathway AKT/G SK-3β/Cdc25A signaling pathway |
Language | English |
LinkModel | DirectLink |
MergedId | FETCHMERGED-LOGICAL-c406t-fa796da9c1bd10d550818e463fa662a4907e6d35f90f8a146e8e087774389fdc3 |
Notes | LncRNAH19; miR-675; hepatocellular carcinoma; migration; invasion; AKT/GSK-313/Cdc25A signaling pathway 42-1679/R Summary: LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for miR-675. However, it is unknown whether LncRNAH19 and miR-675 are involved in the migration and invasion of hepatocellular carcinoma (HCC) cells. The purpose of this study was to investigate the effect and mechanism of LncRNAH19 and miR-675 on migration and invasion of HCC cells. The migration and invasion of HCC cells were measured by Transwell migration and invasion assays after transfection of HCC cells with miR-675 inhibitors and LncRNAH19siRNA. The levels of LncRNAH19 and miR-675 were detected by quantitative reverse transcriptase real-time polymerase chain reaction (qRT-PCR), and the protein expression of AKT, GSK-3[3 and Cdc25A by Western blotting analysis. The expression levels of LncRNAHI9 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the migration of HCC cells (P〈0.01) as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the invasion of HCC cells (P〈0.01) as compared with the control group. Western blotting analy- sis showed that the expression levels of AKT and Cdc25A were significantly increased (P〈0.05), and the expression level of GSK-313 was significantly decreased (P〈0.05) after treatment with miR-675 inhibitors and LncRNAH19siRNA as compared with the control group. These findings suggested that inhibition of LncRNAH 19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3[3/Cdc25A signaling pathway. Jun LV , Ling MA ,Xi-lin CHEN , Xiao-hui HUANG , Qian WANG ( 1Department of Hepatobiliary Surgery, 2Department of Surgical Laboratory, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China 3Department of Hepatobiliary Surgery, the Affiliated Hospital of Guilin Medical College, Guilin 541001, China) ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
PMID | 24939300 |
PQID | 1537592601 |
PQPubID | 23479 |
PageCount | 7 |
ParticipantIDs | wanfang_journals_tjykdxxb_e201403011 proquest_miscellaneous_1537592601 pubmed_primary_24939300 crossref_primary_10_1007_s11596_014_1284_2 crossref_citationtrail_10_1007_s11596_014_1284_2 springer_journals_10_1007_s11596_014_1284_2 chongqing_primary_49956835 |
PublicationCentury | 2000 |
PublicationDate | 2014-06-01 |
PublicationDateYYYYMMDD | 2014-06-01 |
PublicationDate_xml | – month: 06 year: 2014 text: 2014-06-01 day: 01 |
PublicationDecade | 2010 |
PublicationPlace | Heidelberg |
PublicationPlace_xml | – name: Heidelberg – name: China |
PublicationSubtitle | Medical Sciences |
PublicationTitle | Journal of Huazhong University of Science and Technology. Medical sciences |
PublicationTitleAbbrev | J. Huazhong Univ. Sci. Technol. [Med. Sci.] |
PublicationTitleAlternate | Journal of Zuazhong University of Science and Technology: Medical Edition |
PublicationTitle_FL | Journal of Huazhong University of Science and Technology(Medical Science) |
PublicationYear | 2014 |
Publisher | Huazhong University of Science and Technology Department of Hepatobiliary Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China Department of Hepatobiliary Surgery, the Affiliated Hospital of Guilin Medical College, Guilin 541001, China%Department of Hepatobiliary Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China%Department of Surgical Laboratory, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China |
Publisher_xml | – name: Huazhong University of Science and Technology – name: Department of Hepatobiliary Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China – name: Department of Hepatobiliary Surgery, the Affiliated Hospital of Guilin Medical College, Guilin 541001, China%Department of Hepatobiliary Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China%Department of Surgical Laboratory, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China |
References | Du, Kong, You (CR19) 2012; 287 Cross, Alessi, Cohen (CR16) 1995; 378 Cai, Cullen (CR14) 2007; 13 Yao, Liang, Huang (CR5) 2010; 51 Xia, Ooi, Hui (CR6) 2012; 7 Blomberg, Hoffmann (CR28) 1999; 19 Lai, Yang, Zhou (CR8) 2012; 29 Tripathi, Shen, Chakraborty (CR27) 2013; 9 Kang, Wei, Honaker (CR17) 2008; 13 Ayesh, Matouk, Schneider (CR22) 2002; 35 Wendel, De Stanchina, Fridman (CR15) 2004; 428 Nakagawa, Chadwick, Peltomaki (CR13) 2001; 98 Kristjánsdóttir, Rudolph (CR18) 2004; 11 Matouk, DeGroot, Mezan (CR10) 2007; 2 Chen, Lp, Cheng (CR12) 2000; 6 Luo, Li, Wang (CR24) 2013; 280 Luo, Li, Wang (CR23) 2013; 333 Wong, Ching, Chan (CR4) 2010; 16 Zhang, Yang, Yuan (CR26) 2013; 34 Esquela-Kerscher, Slack (CR2) 2006; 6 Molinari, Mercurio, Dominguez (CR29) 2000; 1 Huarte, Rinn (CR7) 2010; 19R2 Geng, Xie, Li (CR9) 2011; 39 Hao, Crenshaw, Moulton (CR25) 1993; 365 Huang, He (CR3) 2011; 104 Cohen, Frame (CR31) 2001; 2 Bartolomei, Zemel, Tilghman (CR21) 1991; 351 Yang, Li, Wang (CR30) 2012; 496 Shtivelman, Sussman, Stokoe (CR33) 2002; 12 Wu, Qin, Li (CR11) 2008; 91 Puc, Keniry, Li (CR32) 2005; 7 Ferlay, Shin, Bray (CR1) 2010; 127 Tsang, Ng, Ng (CR20) 2010; 31 MC Lai (1284_CR8) 2012; 29 V Tripathi (1284_CR27) 2013; 9 YJ Geng (1284_CR9) 2011; 39 P Cohen (1284_CR31) 2001; 2 X Cai (1284_CR14) 2007; 13 T Kang (1284_CR17) 2008; 13 I Blomberg (1284_CR28) 1999; 19 K Kristjánsdóttir (1284_CR18) 2004; 11 MS Bartolomei (1284_CR21) 1991; 351 IJ Matouk (1284_CR10) 2007; 2 Y Du (1284_CR19) 2012; 287 C Yang (1284_CR30) 2012; 496 Y Hao (1284_CR25) 1993; 365 QW Wong (1284_CR4) 2010; 16 A Esquela-Kerscher (1284_CR2) 2006; 6 M Luo (1284_CR24) 2013; 280 S Huang (1284_CR3) 2011; 104 J Puc (1284_CR32) 2005; 7 HG Wendel (1284_CR15) 2004; 428 M Luo (1284_CR23) 2013; 333 CL Chen (1284_CR12) 2000; 6 L Zhang (1284_CR26) 2013; 34 H Xia (1284_CR6) 2012; 7 S Ayesh (1284_CR22) 2002; 35 E Shtivelman (1284_CR33) 2002; 12 J Yao (1284_CR5) 2010; 51 DA Cross (1284_CR16) 1995; 378 H Nakagawa (1284_CR13) 2001; 98 J Ferlay (1284_CR1) 2010; 127 J Wu (1284_CR11) 2008; 91 M Molinari (1284_CR29) 2000; 1 WP Tsang (1284_CR20) 2010; 31 M Huarte (1284_CR7) 2010; 19R2 23222811 - Carcinogenesis. 2013 Mar;34(3):577-86 23399020 - FEBS J. 2013 Apr;280(7):1709-16 15710331 - Cancer Cell. 2005 Feb;7(2):193-204 17237358 - RNA. 2007 Mar;13(3):313-6 19926638 - Carcinogenesis. 2010 Mar;31(3):350-8 22685290 - J Biol Chem. 2012 Jul 27;287(31):26302-11 11120891 - Proc Natl Acad Sci U S A. 2001 Jan 16;98 (2):591-6 1709450 - Nature. 1991 May 9;351(6322):153-5 7692308 - Nature. 1993 Oct 21;365(6448):764-7 22285928 - Gene. 2012 Mar 15;496(1):8-16 20054866 - Hepatology. 2010 Mar;51(3):846-56 8524413 - Nature. 1995 Dec 21-28;378(6559):785-9 20103675 - Clin Cancer Res. 2010 Feb 1;16(3):867-75 17786216 - PLoS One. 2007 Sep 05;2(9):e845 12062056 - Curr Biol. 2002 Jun 4;12 (11):919-24 12325036 - Mol Carcinog. 2002 Oct;35(2):63-74 23555285 - PLoS Genet. 2013 Mar;9(3):e1003368 10454565 - Mol Cell Biol. 1999 Sep;19(9):6183-94 15324805 - Chem Biol. 2004 Aug;11(8):1043-51 18358696 - Genomics. 2008 May;91(5):443-50 18167338 - Cancer Cell. 2008 Jan;13(1):36-47 23354591 - Cancer Lett. 2013 Jun 10;333(2):213-21 21351269 - Int J Cancer. 2010 Dec 15;127(12):2893-917 20729297 - Hum Mol Genet. 2010 Oct 15;19(R2):R152-61 16557279 - Nat Rev Cancer. 2006 Apr;6(4):259-69 22962603 - PLoS One. 2012;7(9):e44206 11256629 - EMBO Rep. 2000 Jul;1(1):71-9 15029198 - Nature. 2004 Mar 18;428(6980):332-7 11584304 - Nat Rev Mol Cell Biol. 2001 Oct;2(10):769-76 10690526 - Clin Cancer Res. 2000 Feb;6(2):474-9 21102580 - Br J Cancer. 2011 Jan 18;104(2):235-40 22289527 - J Int Med Res. 2011;39(6):2119-28 21678027 - Med Oncol. 2012 Sep;29(3):1810-6 |
References_xml | – volume: 13 start-page: 36 issue: 1 year: 2008 end-page: 47 ident: CR17 article-title: GSK-3 beta targets Cdc25A for ubiquitin-mediated proteolysis, and GSK-3 beta inactivation correlates with Cdc25A overproduction in human cancers publication-title: Cancer Cell doi: 10.1016/j.ccr.2007.12.002 – volume: 2 start-page: e845 issue: 9 year: 2007 ident: CR10 article-title: The H19 non-coding RNA is essential for human tumor growth publication-title: PLoS One doi: 10.1371/journal.pone.0000845 – volume: 127 start-page: 2893 issue: 12 year: 2010 end-page: 2917 ident: CR1 article-title: Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008 publication-title: Int J Cancer doi: 10.1002/ijc.25516 – volume: 35 start-page: 63 issue: 2 year: 2002 end-page: 74 ident: CR22 article-title: Possible physiological role of H19 RNA publication-title: Mol Carcinog doi: 10.1002/mc.10075 – volume: 428 start-page: 332 issue: 6980 year: 2004 end-page: 337 ident: CR15 article-title: Survival signaling by Akt and eIF4E in oncogenesis and cancer therapy publication-title: Nature doi: 10.1038/nature02369 – volume: 13 start-page: 313 issue: 3 year: 2007 end-page: 316 ident: CR14 article-title: The imprinted H19 noncoding RNA is a primary micro-RNA precursor publication-title: RNA doi: 10.1261/rna.351707 – volume: 6 start-page: 259 issue: 4 year: 2006 end-page: 269 ident: CR2 article-title: Oncomirs-microRNAs with a role in cancer publication-title: Nat Rev Cancer doi: 10.1038/nrc1840 – volume: 19 start-page: 6183 issue: 9 year: 1999 end-page: 6194 ident: CR28 article-title: Ectopic expression of Cdc25A accelerates the G(1)/S transition and leads to premature activation of cyclin E- and cyclin A-dependent kinases publication-title: Mol Cell Biol – volume: 280 start-page: 1709 issue: 7 year: 2013 end-page: 1716 ident: CR24 article-title: Upregulated H19 contributes to bladder cancer cell proliferation by regulating ID2 expression publication-title: FEBS J doi: 10.1111/febs.12185 – volume: 365 start-page: 764 issue: 6448 year: 1993 end-page: 767 ident: CR25 article-title: Tumour-suppressor activity of H19 RNA publication-title: Nature doi: 10.1038/365764a0 – volume: 287 start-page: 26302 issue: 31 year: 2012 end-page: 26311 ident: CR19 article-title: Elevation of highly up-regulated in liver cancer (HULC) by hepatitis B virus x protein promotes hepatoma cell proliferation via down-regulating p18 publication-title: J Biol Chem doi: 10.1074/jbc.M112.342113 – volume: 9 start-page: e1003368 issue: 3 year: 2013 ident: CR27 article-title: Long noncoding RNA MALAT1 controls cell cycle progression by regulating the expression of oncogenic transcription factor B-MYB publication-title: PLoS Genet doi: 10.1371/journal.pgen.1003368 – volume: 31 start-page: 350 issue: 3 year: 2010 end-page: 358 ident: CR20 article-title: Oncofetal H19-derived miR-675 regulates tumor suppressor RB in human colorectal cancer publication-title: Carcinogenesis doi: 10.1093/carcin/bgp181 – volume: 2 start-page: 769 issue: 10 year: 2001 end-page: 776 ident: CR31 article-title: The renaissance of GSK3 publication-title: Nat Rev Mol Cell Biol doi: 10.1038/35096075 – volume: 29 start-page: 1810 issue: 3 year: 2012 end-page: 1816 ident: CR8 article-title: Long non-coding RNA MALAT-1 overexpression predicts tumor recurrence of hepatocellular carcinoma after liver transplantation publication-title: Med Oncol doi: 10.1007/s12032-011-0004-z – volume: 12 start-page: 919 issue: 11 year: 2002 end-page: 924 ident: CR33 article-title: A role for PI3-kinase and PKB activity in the G2/M phase of the cell cycle publication-title: Curr Biol doi: 10.1016/S0960-9822(02)00843-6 – volume: 1 start-page: 71 issue: 1 year: 2000 end-page: 79 ident: CR29 article-title: Human Cdc25A inactivation in response to S phase inhibition and its role in preventing premature mitosis publication-title: EMBO Rep doi: 10.1093/embo-reports/kvd018 – volume: 6 start-page: 474 issue: 2 year: 2000 end-page: 479 ident: CR12 article-title: Loss of imprinting of the IGF-II and H19 genes in epithelial ovarian cancer publication-title: Clin Cancer Res – volume: 496 start-page: 8 issue: 1 year: 2012 end-page: 16 ident: CR30 article-title: Long non-coding RNA UCA1 regulated cell cycle distribution via CREB through PI3-K dependent pathway in bladder carcinoma cells publication-title: Gene doi: 10.1016/j.gene.2012.01.012 – volume: 39 start-page: 2119 issue: 6 year: 2011 end-page: 2128 ident: CR9 article-title: Large intervening non-coding RNAHOTAIR is associated with hepatocellular carcinoma progression publication-title: J Int Med Res doi: 10.1177/147323001103900608 – volume: 91 start-page: 443 issue: 5 year: 2008 end-page: 450 ident: CR11 article-title: Hypomethylated and hypermethylated profiles of H19DMR are associated with the aberrant imprinting of IGF2 and H19 in human hepatocellular carcinoma publication-title: Genomics doi: 10.1016/j.ygeno.2008.01.007 – volume: 16 start-page: 867 issue: 3 year: 2010 end-page: 875 ident: CR4 article-title: MiR-222 overexpression confers cell migratory advantages in hepatocellular carcinoma through enhancing AKT signaling publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-09-1840 – volume: 7 start-page: e44206 issue: 9 year: 2012 ident: CR6 article-title: MiR-214 targets β-catenin pathway to suppress invasion, stem-like traits and recurrence of human hepatocellular carcinoma publication-title: PLoS One doi: 10.1371/journal.pone.0044206 – volume: 104 start-page: 235 issue: 2 year: 2011 end-page: 240 ident: CR3 article-title: The role of microRNAs in liver cancer progression publication-title: Br J Cancer doi: 10.1038/sj.bjc.6606010 – volume: 51 start-page: 846 issue: 3 year: 2010 end-page: 856 ident: CR5 article-title: MicroRNA-30d promotes tumor invasion and metastasis by targeting Galphai2 in hepatocellular carcinoma publication-title: Hepatology – volume: 19R2 start-page: 152 year: 2010 end-page: 161 ident: CR7 article-title: Large non-coding RNAs: missing links in cancer? publication-title: Hum Mol Genet doi: 10.1093/hmg/ddq353 – volume: 351 start-page: 153 issue: 6322 year: 1991 end-page: 155 ident: CR21 article-title: Parental imprinting of the mouse H19 gene publication-title: Nature doi: 10.1038/351153a0 – volume: 98 start-page: 591 issue: 2 year: 2001 end-page: 596 ident: CR13 article-title: Loss of imprinting of the insulin-like growth factor II gene occurs by biallelic methylation in a core region of H19-associated CTCF-binding sites in colorectal cancer publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.98.2.591 – volume: 333 start-page: 213 issue: 2 year: 2013 end-page: 221 ident: CR23 article-title: Long non-coding RNA H19 increases bladder cancer metastasis by associating with EZH2 and inhibiting E-cadherin expression publication-title: Cancer Lett doi: 10.1016/j.canlet.2013.01.033 – volume: 7 start-page: 193 issue: 2 year: 2005 end-page: 204 ident: CR32 article-title: Lack of PTEN sequesters CHK1 and initiates genetic instability publication-title: Cancer Cell doi: 10.1016/j.ccr.2005.01.009 – volume: 11 start-page: 1043 issue: 8 year: 2004 end-page: 1051 ident: CR18 article-title: Cdc25 phosphatases and cancer publication-title: Chem Biol doi: 10.1016/j.chembiol.2004.07.007 – volume: 34 start-page: 577 issue: 3 year: 2013 end-page: 586 ident: CR26 article-title: Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma publication-title: Carcinogenesis doi: 10.1093/carcin/bgs381 – volume: 378 start-page: 785 issue: 6559 year: 1995 end-page: 789 ident: CR16 article-title: Inhibition of glycogen synthase kinase-3 by insulin mediated by protein kinase B publication-title: Nature doi: 10.1038/378785a0 – volume: 11 start-page: 1043 issue: 8 year: 2004 ident: 1284_CR18 publication-title: Chem Biol doi: 10.1016/j.chembiol.2004.07.007 – volume: 7 start-page: e44206 issue: 9 year: 2012 ident: 1284_CR6 publication-title: PLoS One doi: 10.1371/journal.pone.0044206 – volume: 31 start-page: 350 issue: 3 year: 2010 ident: 1284_CR20 publication-title: Carcinogenesis doi: 10.1093/carcin/bgp181 – volume: 12 start-page: 919 issue: 11 year: 2002 ident: 1284_CR33 publication-title: Curr Biol doi: 10.1016/S0960-9822(02)00843-6 – volume: 13 start-page: 313 issue: 3 year: 2007 ident: 1284_CR14 publication-title: RNA doi: 10.1261/rna.351707 – volume: 280 start-page: 1709 issue: 7 year: 2013 ident: 1284_CR24 publication-title: FEBS J doi: 10.1111/febs.12185 – volume: 2 start-page: 769 issue: 10 year: 2001 ident: 1284_CR31 publication-title: Nat Rev Mol Cell Biol doi: 10.1038/35096075 – volume: 351 start-page: 153 issue: 6322 year: 1991 ident: 1284_CR21 publication-title: Nature doi: 10.1038/351153a0 – volume: 19 start-page: 6183 issue: 9 year: 1999 ident: 1284_CR28 publication-title: Mol Cell Biol doi: 10.1128/MCB.19.9.6183 – volume: 29 start-page: 1810 issue: 3 year: 2012 ident: 1284_CR8 publication-title: Med Oncol doi: 10.1007/s12032-011-0004-z – volume: 378 start-page: 785 issue: 6559 year: 1995 ident: 1284_CR16 publication-title: Nature doi: 10.1038/378785a0 – volume: 6 start-page: 259 issue: 4 year: 2006 ident: 1284_CR2 publication-title: Nat Rev Cancer doi: 10.1038/nrc1840 – volume: 91 start-page: 443 issue: 5 year: 2008 ident: 1284_CR11 publication-title: Genomics doi: 10.1016/j.ygeno.2008.01.007 – volume: 365 start-page: 764 issue: 6448 year: 1993 ident: 1284_CR25 publication-title: Nature doi: 10.1038/365764a0 – volume: 333 start-page: 213 issue: 2 year: 2013 ident: 1284_CR23 publication-title: Cancer Lett doi: 10.1016/j.canlet.2013.01.033 – volume: 51 start-page: 846 issue: 3 year: 2010 ident: 1284_CR5 publication-title: Hepatology doi: 10.1002/hep.23443 – volume: 496 start-page: 8 issue: 1 year: 2012 ident: 1284_CR30 publication-title: Gene doi: 10.1016/j.gene.2012.01.012 – volume: 16 start-page: 867 issue: 3 year: 2010 ident: 1284_CR4 publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-09-1840 – volume: 127 start-page: 2893 issue: 12 year: 2010 ident: 1284_CR1 publication-title: Int J Cancer doi: 10.1002/ijc.25516 – volume: 39 start-page: 2119 issue: 6 year: 2011 ident: 1284_CR9 publication-title: J Int Med Res doi: 10.1177/147323001103900608 – volume: 104 start-page: 235 issue: 2 year: 2011 ident: 1284_CR3 publication-title: Br J Cancer doi: 10.1038/sj.bjc.6606010 – volume: 98 start-page: 591 issue: 2 year: 2001 ident: 1284_CR13 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.98.2.591 – volume: 1 start-page: 71 issue: 1 year: 2000 ident: 1284_CR29 publication-title: EMBO Rep doi: 10.1093/embo-reports/kvd018 – volume: 6 start-page: 474 issue: 2 year: 2000 ident: 1284_CR12 publication-title: Clin Cancer Res – volume: 35 start-page: 63 issue: 2 year: 2002 ident: 1284_CR22 publication-title: Mol Carcinog doi: 10.1002/mc.10075 – volume: 9 start-page: e1003368 issue: 3 year: 2013 ident: 1284_CR27 publication-title: PLoS Genet doi: 10.1371/journal.pgen.1003368 – volume: 34 start-page: 577 issue: 3 year: 2013 ident: 1284_CR26 publication-title: Carcinogenesis doi: 10.1093/carcin/bgs381 – volume: 287 start-page: 26302 issue: 31 year: 2012 ident: 1284_CR19 publication-title: J Biol Chem doi: 10.1074/jbc.M112.342113 – volume: 13 start-page: 36 issue: 1 year: 2008 ident: 1284_CR17 publication-title: Cancer Cell doi: 10.1016/j.ccr.2007.12.002 – volume: 7 start-page: 193 issue: 2 year: 2005 ident: 1284_CR32 publication-title: Cancer Cell doi: 10.1016/j.ccr.2005.01.009 – volume: 19R2 start-page: 152 year: 2010 ident: 1284_CR7 publication-title: Hum Mol Genet doi: 10.1093/hmg/ddq353 – volume: 2 start-page: e845 issue: 9 year: 2007 ident: 1284_CR10 publication-title: PLoS One doi: 10.1371/journal.pone.0000845 – volume: 428 start-page: 332 issue: 6980 year: 2004 ident: 1284_CR15 publication-title: Nature doi: 10.1038/nature02369 – reference: 8524413 - Nature. 1995 Dec 21-28;378(6559):785-9 – reference: 23354591 - Cancer Lett. 2013 Jun 10;333(2):213-21 – reference: 11120891 - Proc Natl Acad Sci U S A. 2001 Jan 16;98 (2):591-6 – reference: 17786216 - PLoS One. 2007 Sep 05;2(9):e845 – reference: 18167338 - Cancer Cell. 2008 Jan;13(1):36-47 – reference: 22285928 - Gene. 2012 Mar 15;496(1):8-16 – reference: 16557279 - Nat Rev Cancer. 2006 Apr;6(4):259-69 – reference: 22289527 - J Int Med Res. 2011;39(6):2119-28 – reference: 1709450 - Nature. 1991 May 9;351(6322):153-5 – reference: 7692308 - Nature. 1993 Oct 21;365(6448):764-7 – reference: 15710331 - Cancer Cell. 2005 Feb;7(2):193-204 – reference: 15029198 - Nature. 2004 Mar 18;428(6980):332-7 – reference: 23399020 - FEBS J. 2013 Apr;280(7):1709-16 – reference: 11584304 - Nat Rev Mol Cell Biol. 2001 Oct;2(10):769-76 – reference: 10690526 - Clin Cancer Res. 2000 Feb;6(2):474-9 – reference: 20729297 - Hum Mol Genet. 2010 Oct 15;19(R2):R152-61 – reference: 18358696 - Genomics. 2008 May;91(5):443-50 – reference: 20054866 - Hepatology. 2010 Mar;51(3):846-56 – reference: 15324805 - Chem Biol. 2004 Aug;11(8):1043-51 – reference: 12062056 - Curr Biol. 2002 Jun 4;12 (11):919-24 – reference: 21678027 - Med Oncol. 2012 Sep;29(3):1810-6 – reference: 10454565 - Mol Cell Biol. 1999 Sep;19(9):6183-94 – reference: 19926638 - Carcinogenesis. 2010 Mar;31(3):350-8 – reference: 22962603 - PLoS One. 2012;7(9):e44206 – reference: 21351269 - Int J Cancer. 2010 Dec 15;127(12):2893-917 – reference: 20103675 - Clin Cancer Res. 2010 Feb 1;16(3):867-75 – reference: 12325036 - Mol Carcinog. 2002 Oct;35(2):63-74 – reference: 23222811 - Carcinogenesis. 2013 Mar;34(3):577-86 – reference: 21102580 - Br J Cancer. 2011 Jan 18;104(2):235-40 – reference: 22685290 - J Biol Chem. 2012 Jul 27;287(31):26302-11 – reference: 11256629 - EMBO Rep. 2000 Jul;1(1):71-9 – reference: 23555285 - PLoS Genet. 2013 Mar;9(3):e1003368 – reference: 17237358 - RNA. 2007 Mar;13(3):313-6 |
SSID | ssj0057624 |
Score | 1.8628613 |
Snippet | Summary: LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for... Summary LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for... LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for miR-675.... |
SourceID | wanfang proquest pubmed crossref springer chongqing |
SourceType | Aggregation Database Index Database Enrichment Source Publisher |
StartPage | 363 |
SubjectTerms | Blotting, Western Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology cdc25 Phosphatases - metabolism Cell Line Cell Line, Tumor Cell Movement - genetics Down-Regulation Gene Expression Regulation, Neoplastic Gene Knockdown Techniques Glycogen Synthase Kinase 3 - metabolism Glycogen Synthase Kinase 3 beta Hep G2 Cells HepG2细胞 Humans Liver Neoplasms - genetics Liver Neoplasms - metabolism Liver Neoplasms - pathology Medicine Medicine & Public Health MicroRNAs - genetics Neoplasm Invasiveness Proto-Oncogene Proteins c-akt - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA Interference RNA, Long Noncoding - genetics Signal Transduction Western印迹 侵袭 信号通路 定量RT-PCR 聚合酶链反应 肝癌细胞 迁移 |
Title | Downregulation of LncRNAH19 and MiR-675 Promotes Migration and Invasion of Human Hepatocellular Carcinoma Cells through AKT/GSK-3β/Cdc25A Signaling Pathway |
URI | http://lib.cqvip.com/qk/85740A/201403/49956835.html https://link.springer.com/article/10.1007/s11596-014-1284-2 https://www.ncbi.nlm.nih.gov/pubmed/24939300 https://www.proquest.com/docview/1537592601 https://d.wanfangdata.com.cn/periodical/tjykdxxb-e201403011 |
Volume | 34 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV3NbtQwELZQKyEuiH9SoDJST6CoSew4yTEqbVeU7aGwUjlZju1sF6hTmhTad-EpeBCeiZnE2S0CVeKaxE7kmczMZ8_MR8iWEpE1qeJhnOko5NzGYSUMoFbNGc9twgqN-5DTQzGZ8bfH6bGv427HbPfxSLK31KtiN_C8iH6xz17OQ7C76ylAd1TrWVKO5hfi54HJVmSYVsnYeJT5rymwocJJ4-Zf4XV_Oqa_os1rJ6V9fY-rlZtfc0V798hdH0PSchD6fXLLugfk9tSfkj8kP94AtD4fSOZh2WlT03dOHx2Wk7igyhk6XRyFEMLTsz4Xz7b0dDEfNKG_vXDfVOsH9hx-9AScVtfgJj9mrVKNBESuOVUUL7XUk_1QCBi3998fhOzXz-0do5O0pJgforDknSL38Xd19YjM9nY_7ExCz8IQanD2XVirrBBGFTquTBwZQDTg4y0XrFZCJIoDurbCsLQuojpXYHhtbvsug8irXhvNHpM11zj7lMA3iUpEjLGaA-xRosgMy02qNYRhxvAsIBtLccizoduG5Fh7C3FiQKJRPlL7_uVIo_FFrjovo3gliFeieGUSkFfLIeN0Nzz8chS6hF8M108521y0EpxClhbYey0gTwZtWE4H6JUVLIoC8npUD-mtQHvTu7a8Bq0e7j5dfTaXl5W0CaJeNLwb_zXpM3IHRw55bM_JWnd-YV9AxNRVm2S93P94sLvZ_ym_Afk9DFI |
linkProvider | Springer Nature |
linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV3bbtNAEF2hVAJeKNficlukPoHcOtn1On6MSttALg8llcrTar27TkPpuq0daPkWvoIP4ZuY8SUpF1Xqa2KP48x4Zo7ncgjZUCKwJlTcb0c68Dm3bT8RBlCr5ox3bYfFGt9Djsaif8A_HIaH9Rx33nS7NyXJ0lMvh90g8iL6xT17Xe6D313hAMHDFlnp7X0a7DQOGDLoistWRNhYyVhTzPyfEFypcJS56Rlc8M_Q9E--eaVWWk74uFS56ZVgtLtKJs1tVD0ox5vzItnU3__a8HjD-7xP7tXJKe1V1vSA3LLuIbk9qsvvj8iPd4DZzyv2etAnzVI6dHp_3Ou3Y6qcoaPZvg_YgJ6WTX42pyezaWVi5dcz91Xl9YklOSA9gmhYZFg9wHZYqpHZyGUniuJHOa1ZhChkolt7Hwc--_Vza9voTtij2HiicJaeIqnyN3X5mBzs7ky2-35N7-BryCIKP1VRLIyKdTsx7cAAVILkwXLBUiVER3GA7VYYFqZxkHYVeHTbteX6QiRsT41mT0jLZc4-JfCbRCICxljKAU8pEUeGdU2oNeR3xvDII-sLLcvTao2H5DjUCwmoR4JG7VLXi9GRn-OLXK50RpVIUIlElciOR94sTmnEXXPw68aWJDy7-P8pZ7N5LiHaRGGMS908slYZ2UIcwGIWsyDwyNvGTGTtXvLrrrVRG-by4OLz5bG5uEik7SCcRo--fiOhr8id_mQ0lMP348EzchelVM1yz0mrOJ_bF5CWFcnL-jH8DQ4cKnQ |
linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV3NbtQwELZQkSouiH9SChipJ1C0Sew4yXHVsiy0u0KFlXqzHNvZbqHOtkmhfReeggfhmZjJz24RqBLXxB5HmfH82DPzEbKjRGBNrLgfJjrwObehnwsDUavmjKc2YpnGc8jJVIxn_MNRfNThnFZ9tnt_JdnWNGCXJlcPlqYYrAvfwApjJIw991Lugw6-Ddo4xJyuWTTsVTH40i2qrUgwxZKx_lrzXySwucJx6eZnsPSfRuovz_ParWlT6-MK5ebXzNLoHrnb-ZN02ArAfXLLugdkc9LdmD8kP_YgzD5vAeeBBbQs6IHTh9PhOMyocoZOFoc-uPN02eTl2YqeLuatVDSvF-6bqrqJDZ4fPQYDVpd44I8ZrFQjGJErTxXFRxXtgH8oOI-Dd5_2ffbr52DX6CgeUswVUVj-ThEH-bu6ekRmo7efd8d-h8jgazD8tV-oJBNGZTrMTRgYiG7A3lsuWKGEiBSHSNsKw-IiC4pUgRK2qW06DiLGemE0e0w2XOnsUwLfJHIRMMYKDiGQElliWGpircElM4YnHtlasUMu284bkmMdLviMHgl6_kjd9TJHSI2vct2FGdkrgb0S2Ssjj7xeTenJ3TD4Vc90CdsN_59ytryoJBiIJM6wD5tHnrTSsCIHkSzLWBB45E0vHrLTCNVNa-10ErQeXJ9cfTGXl7m0EUbAqIS3_ovoS7L5cW8kD95P95-RO0ikTW_bJhv1-YV9Do5Unb9oNstvvkcR7Q |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Downregulation+of+LncRNAH19+and+MiR-675+promotes+migration+and+invasion+of+human+hepatocellular+carcinoma+cells+through+AKT%2FGSK-3%CE%B2%2FCdc25A+signaling+pathway&rft.jtitle=Journal+of+Huazhong+University+of+Science+and+Technology.+Medical+sciences&rft.au=Lv%2C+Jun&rft.au=Ma%2C+Ling&rft.au=Chen%2C+Xi-lin&rft.au=Huang%2C+Xiao-hui&rft.date=2014-06-01&rft.issn=1672-0733&rft.eissn=1993-1352&rft.volume=34&rft.issue=3&rft.spage=363&rft.epage=369&rft_id=info:doi/10.1007%2Fs11596-014-1284-2&rft.externalDBID=n%2Fa&rft.externalDocID=10_1007_s11596_014_1284_2 |
thumbnail_s | http://utb.summon.serialssolutions.com/2.0.0/image/custom?url=http%3A%2F%2Fimage.cqvip.com%2Fvip1000%2Fqk%2F85740A%2F85740A.jpg http://utb.summon.serialssolutions.com/2.0.0/image/custom?url=http%3A%2F%2Fwww.wanfangdata.com.cn%2Fimages%2FPeriodicalImages%2Ftjykdxxb-e%2Ftjykdxxb-e.jpg |