miR-589 promotes gastric cancer aggressiveness by a LIFR-PI3K/AKT-c-Jun regulatory feedback loop

As novel biomarkers for various cancers, microRNAs negatively regulate genes expression via promoting mRNA degradation and suppressing mRNA translation. miR-589 has been reported to be deregulated in several human cancer types. However, its biological role has not been functionally characterized in...

Full description

Saved in:
Bibliographic Details
Published inJournal of experimental & clinical cancer research Vol. 37; no. 1; pp. 152 - 11
Main Authors Zhang, Feifei, Li, Kaitao, Pan, Mingxin, Li, Weidong, Wu, Juan, Li, Mingyi, Zhao, Liang, Wang, Hui
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 16.07.2018
BioMed Central
BMC
Subjects
Analysis
Animals
Breast cancer
Cell growth
Cell Line, Tumor
Cytokines
Development and progression
DNA methylation
Experiments
Feedback
Feedback loop
Female
Gastric cancer
Gene expression
Genetic aspects
Health aspects
Humans
Kinases
Laboratories
Leukemia
LIFR
Liver cancer
Male
Medical prognosis
Metastasis
Mice
Mice, Nude
MicroRNA
MicroRNAs
MicroRNAs - metabolism
miR-589
Neoplasm Metastasis
Phosphatidylinositol 3-Kinases - metabolism
Physiological aspects
Proteins
Proto-Oncogene Proteins c-akt - metabolism
Stomach cancer
Stomach Neoplasms - genetics
Stomach Neoplasms - pathology
Tumorigenesis
China
United States > US
Feedback loop
LIFR
miR-589
Metastasis
Gastric cancer
Online AccessGet full text

Cover

Abstract As novel biomarkers for various cancers, microRNAs negatively regulate genes expression via promoting mRNA degradation and suppressing mRNA translation. miR-589 has been reported to be deregulated in several human cancer types. However, its biological role has not been functionally characterized in gastric cancer. Here, we aim to investigate the biological effect of miR-589 on gastric cancer and to reveal the possible mechanism. Real-time PCR was performed to evaluate the expression of miR-589 in 34 paired normal and stomach tumor specimens, as well as gastric cell lines. Functional assays, such as wound healing, transwell assays and in vivo assays, were used to detect the biological effect of miR-589 and LIFR. We determined the role of miR-589 in gastric cancer tumorigenesis in vivo using xenograft nude models. Dual-luciferase report assays and Chromatin immunoprecipitation (ChIP) assay were performed for target evaluation, and the relationships were confirmed by western blot assay. MiR-589 expression was significantly higher in tumor tissues and gastric cancer cells than those in matched normal tissues and gastric epithelial cells, respectively. Clinically, overexpression of miR-589 is associated with tumor metastasis, invasion and poor prognosis of GC patients. Gain- and loss-of function experiments showed that miR-589 promoted cell migration, metastasis and invasion in vitro and lung metastasis in vivo. Mechanistically, we found that miR-589 directly targeted LIFR to activate PI3K/AKT/c-Jun signaling. Meanwhile, c-Jun bound to the promoter region of miR-589 and activated its transcription. Thus miR-589 regulated its expression in a feedback loop that promoted cell migration, metastasis and invasion. Our study identified miR-589, as an oncogene, markedly induced cell metastasis and invasion via an atypical miR-589-LIFR-PI3K/AKT-c-Jun feedback loop, which suggested miR-589 as a potential biomarker and/or therapeutic target for the gastric cancer management.
AbstractList As novel biomarkers for various cancers, microRNAs negatively regulate genes expression via promoting mRNA degradation and suppressing mRNA translation. miR-589 has been reported to be deregulated in several human cancer types. However, its biological role has not been functionally characterized in gastric cancer. Here, we aim to investigate the biological effect of miR-589 on gastric cancer and to reveal the possible mechanism. Real-time PCR was performed to evaluate the expression of miR-589 in 34 paired normal and stomach tumor specimens, as well as gastric cell lines. Functional assays, such as wound healing, transwell assays and in vivo assays, were used to detect the biological effect of miR-589 and LIFR. We determined the role of miR-589 in gastric cancer tumorigenesis in vivo using xenograft nude models. Dual-luciferase report assays and Chromatin immunoprecipitation (ChIP) assay were performed for target evaluation, and the relationships were confirmed by western blot assay. MiR-589 expression was significantly higher in tumor tissues and gastric cancer cells than those in matched normal tissues and gastric epithelial cells, respectively. Clinically, overexpression of miR-589 is associated with tumor metastasis, invasion and poor prognosis of GC patients. Gain- and loss-of function experiments showed that miR-589 promoted cell migration, metastasis and invasion in vitro and lung metastasis in vivo. Mechanistically, we found that miR-589 directly targeted LIFR to activate PI3K/AKT/c-Jun signaling. Meanwhile, c-Jun bound to the promoter region of miR-589 and activated its transcription. Thus miR-589 regulated its expression in a feedback loop that promoted cell migration, metastasis and invasion. Our study identified miR-589, as an oncogene, markedly induced cell metastasis and invasion via an atypical miR-589-LIFR-PI3K/AKT-c-Jun feedback loop, which suggested miR-589 as a potential biomarker and/or therapeutic target for the gastric cancer management.
As novel biomarkers for various cancers, microRNAs negatively regulate genes expression via promoting mRNA degradation and suppressing mRNA translation. miR-589 has been reported to be deregulated in several human cancer types. However, its biological role has not been functionally characterized in gastric cancer. Here, we aim to investigate the biological effect of miR-589 on gastric cancer and to reveal the possible mechanism.BACKGROUNDAs novel biomarkers for various cancers, microRNAs negatively regulate genes expression via promoting mRNA degradation and suppressing mRNA translation. miR-589 has been reported to be deregulated in several human cancer types. However, its biological role has not been functionally characterized in gastric cancer. Here, we aim to investigate the biological effect of miR-589 on gastric cancer and to reveal the possible mechanism.Real-time PCR was performed to evaluate the expression of miR-589 in 34 paired normal and stomach tumor specimens, as well as gastric cell lines. Functional assays, such as wound healing, transwell assays and in vivo assays, were used to detect the biological effect of miR-589 and LIFR. We determined the role of miR-589 in gastric cancer tumorigenesis in vivo using xenograft nude models. Dual-luciferase report assays and Chromatin immunoprecipitation (ChIP) assay were performed for target evaluation, and the relationships were confirmed by western blot assay.METHODSReal-time PCR was performed to evaluate the expression of miR-589 in 34 paired normal and stomach tumor specimens, as well as gastric cell lines. Functional assays, such as wound healing, transwell assays and in vivo assays, were used to detect the biological effect of miR-589 and LIFR. We determined the role of miR-589 in gastric cancer tumorigenesis in vivo using xenograft nude models. Dual-luciferase report assays and Chromatin immunoprecipitation (ChIP) assay were performed for target evaluation, and the relationships were confirmed by western blot assay.MiR-589 expression was significantly higher in tumor tissues and gastric cancer cells than those in matched normal tissues and gastric epithelial cells, respectively. Clinically, overexpression of miR-589 is associated with tumor metastasis, invasion and poor prognosis of GC patients. Gain- and loss-of function experiments showed that miR-589 promoted cell migration, metastasis and invasion in vitro and lung metastasis in vivo. Mechanistically, we found that miR-589 directly targeted LIFR to activate PI3K/AKT/c-Jun signaling. Meanwhile, c-Jun bound to the promoter region of miR-589 and activated its transcription. Thus miR-589 regulated its expression in a feedback loop that promoted cell migration, metastasis and invasion.RESULTMiR-589 expression was significantly higher in tumor tissues and gastric cancer cells than those in matched normal tissues and gastric epithelial cells, respectively. Clinically, overexpression of miR-589 is associated with tumor metastasis, invasion and poor prognosis of GC patients. Gain- and loss-of function experiments showed that miR-589 promoted cell migration, metastasis and invasion in vitro and lung metastasis in vivo. Mechanistically, we found that miR-589 directly targeted LIFR to activate PI3K/AKT/c-Jun signaling. Meanwhile, c-Jun bound to the promoter region of miR-589 and activated its transcription. Thus miR-589 regulated its expression in a feedback loop that promoted cell migration, metastasis and invasion.Our study identified miR-589, as an oncogene, markedly induced cell metastasis and invasion via an atypical miR-589-LIFR-PI3K/AKT-c-Jun feedback loop, which suggested miR-589 as a potential biomarker and/or therapeutic target for the gastric cancer management.CONCLUSIONOur study identified miR-589, as an oncogene, markedly induced cell metastasis and invasion via an atypical miR-589-LIFR-PI3K/AKT-c-Jun feedback loop, which suggested miR-589 as a potential biomarker and/or therapeutic target for the gastric cancer management.
Abstract Background As novel biomarkers for various cancers, microRNAs negatively regulate genes expression via promoting mRNA degradation and suppressing mRNA translation. miR-589 has been reported to be deregulated in several human cancer types. However, its biological role has not been functionally characterized in gastric cancer. Here, we aim to investigate the biological effect of miR-589 on gastric cancer and to reveal the possible mechanism. Methods Real-time PCR was performed to evaluate the expression of miR-589 in 34 paired normal and stomach tumor specimens, as well as gastric cell lines. Functional assays, such as wound healing, transwell assays and in vivo assays, were used to detect the biological effect of miR-589 and LIFR. We determined the role of miR-589 in gastric cancer tumorigenesis in vivo using xenograft nude models. Dual-luciferase report assays and Chromatin immunoprecipitation (ChIP) assay were performed for target evaluation, and the relationships were confirmed by western blot assay. Result MiR-589 expression was significantly higher in tumor tissues and gastric cancer cells than those in matched normal tissues and gastric epithelial cells, respectively. Clinically, overexpression of miR-589 is associated with tumor metastasis, invasion and poor prognosis of GC patients. Gain- and loss-of function experiments showed that miR-589 promoted cell migration, metastasis and invasion in vitro and lung metastasis in vivo. Mechanistically, we found that miR-589 directly targeted LIFR to activate PI3K/AKT/c-Jun signaling. Meanwhile, c-Jun bound to the promoter region of miR-589 and activated its transcription. Thus miR-589 regulated its expression in a feedback loop that promoted cell migration, metastasis and invasion. Conclusion Our study identified miR-589, as an oncogene, markedly induced cell metastasis and invasion via an atypical miR-589-LIFR-PI3K/AKT-c-Jun feedback loop, which suggested miR-589 as a potential biomarker and/or therapeutic target for the gastric cancer management.
Background As novel biomarkers for various cancers, microRNAs negatively regulate genes expression via promoting mRNA degradation and suppressing mRNA translation. miR-589 has been reported to be deregulated in several human cancer types. However, its biological role has not been functionally characterized in gastric cancer. Here, we aim to investigate the biological effect of miR-589 on gastric cancer and to reveal the possible mechanism. Methods Real-time PCR was performed to evaluate the expression of miR-589 in 34 paired normal and stomach tumor specimens, as well as gastric cell lines. Functional assays, such as wound healing, transwell assays and in vivo assays, were used to detect the biological effect of miR-589 and LIFR. We determined the role of miR-589 in gastric cancer tumorigenesis in vivo using xenograft nude models. Dual-luciferase report assays and Chromatin immunoprecipitation (ChIP) assay were performed for target evaluation, and the relationships were confirmed by western blot assay. Result MiR-589 expression was significantly higher in tumor tissues and gastric cancer cells than those in matched normal tissues and gastric epithelial cells, respectively. Clinically, overexpression of miR-589 is associated with tumor metastasis, invasion and poor prognosis of GC patients. Gain- and loss-of function experiments showed that miR-589 promoted cell migration, metastasis and invasion in vitro and lung metastasis in vivo. Mechanistically, we found that miR-589 directly targeted LIFR to activate PI3K/AKT/c-Jun signaling. Meanwhile, c-Jun bound to the promoter region of miR-589 and activated its transcription. Thus miR-589 regulated its expression in a feedback loop that promoted cell migration, metastasis and invasion. Conclusion Our study identified miR-589, as an oncogene, markedly induced cell metastasis and invasion via an atypical miR-589-LIFR-PI3K/AKT-c-Jun feedback loop, which suggested miR-589 as a potential biomarker and/or therapeutic target for the gastric cancer management. Keywords: miR-589, Gastric cancer, LIFR, Metastasis, Feedback loop
LIFR has been identified as a metastasis suppressor of breast cancer via the HIPPO-YAP pathway. [...]LIFR expression is down regulated in breast cancer and also significantly correlates with poor prognosis and overall survival outcomes of breast cancer patients [18–20]. [...]Real-time PCR analysis showed a relatively low miR-589 expression in cells treated with c-Jun siRNAs (Fig. 6c). [...]LY294002 and LIFR overexpression significantly decreased miR-589 expression (Fig. 6a & b), suggesting the existence of a miR-589-LIFR-PI3K/AKT-c-Jun regulatory feedback loop. In agreement with this findings, we found that treatment with LY294002 triggered a decrease in c-Jun expression in GC cells, whereas, we did not detect the change of JNK expression after using LY294002. [...]extensive study is required to examine whether LY294002 reduce c-Jun expression through AKT/JNK/c-Jun signaling. Interestingly, c-Jun inversely bound to the promoter region of miR-589 and activated its transcription. [...]miR-589 does not induce gastric carcinogenesis alone, instead, miR-589 forms a miR-589-LIFR-PI3K/AKT-c-Jun feedback loop which contributes to cell migration, metastasis and invasion.
As novel biomarkers for various cancers, microRNAs negatively regulate genes expression via promoting mRNA degradation and suppressing mRNA translation. miR-589 has been reported to be deregulated in several human cancer types. However, its biological role has not been functionally characterized in gastric cancer. Here, we aim to investigate the biological effect of miR-589 on gastric cancer and to reveal the possible mechanism. Real-time PCR was performed to evaluate the expression of miR-589 in 34 paired normal and stomach tumor specimens, as well as gastric cell lines. Functional assays, such as wound healing, transwell assays and in vivo assays, were used to detect the biological effect of miR-589 and LIFR. We determined the role of miR-589 in gastric cancer tumorigenesis in vivo using xenograft nude models. Dual-luciferase report assays and Chromatin immunoprecipitation (ChIP) assay were performed for target evaluation, and the relationships were confirmed by western blot assay. MiR-589 expression was significantly higher in tumor tissues and gastric cancer cells than those in matched normal tissues and gastric epithelial cells, respectively. Clinically, overexpression of miR-589 is associated with tumor metastasis, invasion and poor prognosis of GC patients. Gain- and loss-of function experiments showed that miR-589 promoted cell migration, metastasis and invasion in vitro and lung metastasis in vivo. Mechanistically, we found that miR-589 directly targeted LIFR to activate PI3K/AKT/c-Jun signaling. Meanwhile, c-Jun bound to the promoter region of miR-589 and activated its transcription. Thus miR-589 regulated its expression in a feedback loop that promoted cell migration, metastasis and invasion. Our study identified miR-589, as an oncogene, markedly induced cell metastasis and invasion via an atypical miR-589-LIFR-PI3K/AKT-c-Jun feedback loop, which suggested miR-589 as a potential biomarker and/or therapeutic target for the gastric cancer management.
ArticleNumber 152
Audience Academic
Author Wu, Juan
Li, Weidong
Wang, Hui
Zhao, Liang
Zhang, Feifei
Pan, Mingxin
Li, Mingyi
Li, Kaitao
Author_xml – sequence: 1
  givenname: Feifei
  surname: Zhang
  fullname: Zhang, Feifei
– sequence: 2
  givenname: Kaitao
  surname: Li
  fullname: Li, Kaitao
– sequence: 3
  givenname: Mingxin
  surname: Pan
  fullname: Pan, Mingxin
– sequence: 4
  givenname: Weidong
  surname: Li
  fullname: Li, Weidong
– sequence: 5
  givenname: Juan
  surname: Wu
  fullname: Wu, Juan
– sequence: 6
  givenname: Mingyi
  surname: Li
  fullname: Li, Mingyi
– sequence: 7
  givenname: Liang
  surname: Zhao
  fullname: Zhao, Liang
– sequence: 8
  givenname: Hui
  surname: Wang
  fullname: Wang, Hui
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30012200$$D View this record in MEDLINE/PubMed
BookMark eNp9km9r1TAUxotM3B_9AL6RgiC-6ZbTJmnyRrgMp9cNlDFfx9M06TLb5i5pB_v25nrnvHeIlJDk9Pc8pz08h9ne6EeTZa-BHAMIfhKhIpQXBERBRAkFfZYdQM14ISXne1vn_ewwxhtCOEiQL7L9ihAoS0IOsh-DuyyYkPkq-MFPJuYdxik4nWsctQk5dl0wMbo7M6Ytb-5zzC-WZ5fFt2V1frI4vyp08WUe82C6ucfJh_vcGtM2qH_mvferl9lzi300rx72o-z72cer08_FxddPy9PFRaGZhKkwCG1rgQtrBJYCWo1NSbWEui2pZZRLqBrJOOoSdd1ogtYaXokS0x15VR1ly41v6_FGrYIbMNwrj079LvjQKQyT071RTDZStA01lgO1lqFJqxEktS4pB528Pmy8VnMzmFabcQrY75juvhndter8neKECsF4Mnj_YBD87WzipAYXtel7HI2foypJDawGIUlC3z5Bb_wcxjSqDUWhpuwv1WH6ATdan_rqtalaMFoTJhmIRB3_g0pPawanU3asS_UdwbstwbXBfrqOvp8n58e4C77ZnsjjKP4EKQGwAXTwMQZjHxEgah1WtQmrSmFV67AqmjT1E412E657p892_X-UvwAbcesP
CitedBy_id crossref_primary_10_2147_OTT_S237356
crossref_primary_10_1158_0008_5472_CAN_18_2900
crossref_primary_10_1111_jcmm_14309
crossref_primary_10_1016_j_aohep_2021_100567
crossref_primary_10_1002_tox_23104
crossref_primary_10_3389_fonc_2021_693724
crossref_primary_10_3390_ijms25105144
crossref_primary_10_1186_s13046_024_02946_8
crossref_primary_10_1186_s13046_024_03055_2
crossref_primary_10_3233_CBM_190571
crossref_primary_10_1016_j_celrep_2020_108327
crossref_primary_10_2147_IJN_S391872
crossref_primary_10_1097_CM9_0000000000000921
crossref_primary_10_1007_s12032_023_01990_2
crossref_primary_10_1080_14737140_2019_1659136
crossref_primary_10_1155_2022_2333848
crossref_primary_10_3892_ijmm_2020_4603
crossref_primary_10_1007_s10120_022_01278_w
crossref_primary_10_18632_aging_202657
crossref_primary_10_1089_dna_2021_0549
crossref_primary_10_3389_fphar_2022_918588
crossref_primary_10_1007_s10616_020_00388_6
crossref_primary_10_1007_s10620_021_07055_6
crossref_primary_10_1016_j_bbcan_2022_188737
crossref_primary_10_1016_j_dci_2020_103642
crossref_primary_10_1016_j_omtn_2020_09_021
crossref_primary_10_3390_cells8111400
crossref_primary_10_3892_ol_2019_10548
crossref_primary_10_1007_s10735_021_10044_8
crossref_primary_10_1016_j_bcp_2020_114384
crossref_primary_10_1038_s41419_021_03576_0
crossref_primary_10_1016_j_canlet_2019_02_042
crossref_primary_10_1007_s10528_022_10248_x
crossref_primary_10_3389_fonc_2022_808174
crossref_primary_10_1002_ijc_35157
crossref_primary_10_1016_j_bcp_2023_115466
crossref_primary_10_1155_2020_2863236
crossref_primary_10_3390_cancers10120475
crossref_primary_10_1177_0300060520903661
crossref_primary_10_1136_jitc_2022_005461
crossref_primary_10_1016_j_cca_2019_07_003
crossref_primary_10_1590_1414_431x20198341
crossref_primary_10_1002_mc_23025
Cites_doi 10.1016/j.suronc.2010.12.004
10.1186/bcr3349
10.1007/s00432-015-2071-6
10.1093/carcin/bgv108
10.1074/jbc.M116.718551
10.1155/2017/7869802
10.1016/j.bbamcr.2006.12.009
10.1186/s13058-017-0865-y
10.1593/neo.13966
10.1016/j.canlet.2017.08.017
10.1016/j.canlet.2009.08.013
10.1016/S0092-8674(04)00045-5
10.1053/j.gastro.2012.05.003
10.1038/nature06487
10.1002/bies.200800212
10.1002/j.1460-2075.1991.tb07833.x
10.1016/j.hep.2003.09.029
10.1038/cddis.2016.225
10.3892/ijo.2017.3967
10.1200/JCO.2014.60.1799
10.1200/JCO.2005.05.0245
10.1002/cncr.27903
10.1038/bjc.2014.14
10.1093/nar/gkt1323
10.1093/hmg/ddx086
10.1039/C3CS60312A
10.1186/1471-2407-7-145
10.1186/s13046-016-0452-6
10.1016/j.ccell.2016.08.001
10.1038/onc.2016.201
10.1146/annurev-pathol-012513-104715
10.1016/S0140-6736(16)30354-3
10.2174/0929867323666160818093854
10.1038/nm.2940
10.3892/ijo.2015.3052
10.1038/ncomms11309
10.1101/gr.219741.116
10.1016/j.ijbiomac.2016.10.026
10.1158/1535-7163.MCT-14-0167
ContentType Journal Article
Copyright COPYRIGHT 2018 BioMed Central Ltd.
Copyright © 2018. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and conditions, you may use this content in accordance with the terms of the License.
The Author(s). 2018
Copyright_xml – notice: COPYRIGHT 2018 BioMed Central Ltd.
– notice: Copyright © 2018. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and conditions, you may use this content in accordance with the terms of the License.
– notice: The Author(s). 2018
DBID AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
3V.
7X7
7XB
88E
8FI
8FJ
8FK
ABUWG
AFKRA
AZQEC
BENPR
CCPQU
DWQXO
FYUFA
GHDGH
K9.
M0S
M1P
PHGZM
PHGZT
PIMPY
PJZUB
PKEHL
PPXIY
PQEST
PQQKQ
PQUKI
PRINS
7X8
5PM
DOA
DOI 10.1186/s13046-018-0821-4
DatabaseName CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
ProQuest Central (Corporate)
Health & Medical Collection
ProQuest Central (purchase pre-March 2016)
Medical Database (Alumni Edition)
ProQuest Hospital Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Central (Alumni)
ProQuest Central UK/Ireland
ProQuest Central Essentials
ProQuest Central
ProQuest One Community College
ProQuest Central Korea
Health Research Premium Collection
Health Research Premium Collection (Alumni)
ProQuest Health & Medical Complete (Alumni)
ProQuest Health & Medical Collection
Medical Database
ProQuest Central Premium
ProQuest One Academic
Publicly Available Content Database
ProQuest Health & Medical Research Collection
ProQuest One Academic Middle East (New)
ProQuest One Health & Nursing
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Academic
ProQuest One Academic UKI Edition
ProQuest Central China
MEDLINE - Academic
PubMed Central (Full Participant titles)
Open Access Journals (DOAJ)
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
Publicly Available Content Database
ProQuest One Academic Middle East (New)
ProQuest Central Essentials
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
ProQuest One Community College
ProQuest One Health & Nursing
ProQuest Central China
ProQuest Central
Health Research Premium Collection
Health and Medicine Complete (Alumni Edition)
ProQuest Central Korea
Health & Medical Research Collection
ProQuest Central (New)
ProQuest Medical Library (Alumni)
ProQuest One Academic Eastern Edition
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
ProQuest Hospital Collection (Alumni)
ProQuest Health & Medical Complete
ProQuest Medical Library
ProQuest One Academic UKI Edition
ProQuest One Academic
ProQuest One Academic (New)
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList MEDLINE
MEDLINE - Academic


Publicly Available Content Database
Database_xml – sequence: 1
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 2
  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: 3
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
– sequence: 4
  dbid: BENPR
  name: ProQuest Central
  url: https://www.proquest.com/central
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 1756-9966
EndPage 11
ExternalDocumentID oai_doaj_org_article_59b98db4ef614ff5aef5ab80fe82461c
PMC6048856
A547059518
30012200
10_1186_s13046_018_0821_4
Genre Journal Article
GeographicLocations China
United States--US
GeographicLocations_xml – name: China
– name: United States--US
GrantInformation_xml – fundername: National Natural Science Foundation of China (CN)
  grantid: Nos. 81572813
– fundername: Zhujiang Star 2015 of Science and Technology Program of Gugangzhou
  grantid: 201506010037
– fundername: National Natural Science Foundation of China
  grantid: Nos. 81773082
– fundername: Higher Education Fund Project of Guangzhou
  grantid: 2012C070
– fundername: Science and Technology Program of Guangzhou
  grantid: 1563000235
– fundername: Guangdong Natural Science Foundation
  grantid: 2015A030313274
– fundername: ;
  grantid: Nos. 81572813
– fundername: ;
  grantid: 2015A030313274
– fundername: ;
  grantid: 2012C070
– fundername: ;
  grantid: Nos. 81773082
– fundername: ;
  grantid: 201506010037
– fundername: ;
  grantid: 1563000235
GroupedDBID ---
0R~
29K
2WC
4.4
5GY
5VS
7X7
88E
8FI
8FJ
AAFWJ
AAJSJ
AASML
AAYXX
ABDBF
ABUWG
ACGFO
ACGFS
ADBBV
ADRAZ
ADUKV
AENEX
AFKRA
AFPKN
AHBYD
AHMBA
AHYZX
ALIPV
ALMA_UNASSIGNED_HOLDINGS
AMKLP
AOIJS
BAWUL
BCNDV
BENPR
BFQNJ
BMC
BPHCQ
BVXVI
C6C
CCPQU
CITATION
CS3
D-I
DIK
DU5
E3Z
EBD
EBLON
EBS
EJD
ESX
F5P
FYUFA
GROUPED_DOAJ
H13
HMCUK
HYE
IAO
IEA
IHR
IHW
INH
INR
ITC
KQ8
M1P
M48
M~E
O5R
O5S
OK1
OVT
P2P
PGMZT
PHGZM
PHGZT
PIMPY
PQQKQ
PROAC
PSQYO
RBZ
RNS
ROL
RPM
RSV
SMD
SOJ
TR2
TUS
UKHRP
~8M
-5E
-5G
-A0
-BR
3V.
ACRMQ
ADINQ
C24
CGR
CUY
CVF
ECM
EIF
NPM
PMFND
7XB
8FK
AZQEC
DWQXO
K9.
PJZUB
PKEHL
PPXIY
PQEST
PQUKI
PRINS
7X8
5PM
PUEGO
ID FETCH-LOGICAL-c591t-ea1ddf168fe8a281dcab24c917d24f546913b956ac2ac7bc0affe6382a2aca633
IEDL.DBID M48
ISSN 1756-9966
0392-9078
IngestDate Wed Aug 27 01:30:21 EDT 2025
Thu Aug 21 14:13:37 EDT 2025
Fri Jul 11 04:40:55 EDT 2025
Fri Jul 25 07:32:05 EDT 2025
Tue Jun 17 20:39:46 EDT 2025
Tue Jun 10 20:46:22 EDT 2025
Thu May 22 21:22:44 EDT 2025
Wed Feb 19 02:32:48 EST 2025
Thu Apr 24 22:58:57 EDT 2025
Tue Jul 01 02:26:32 EDT 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 1
Keywords Feedback loop
LIFR
miR-589
Metastasis
Gastric cancer
Language English
License Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c591t-ea1ddf168fe8a281dcab24c917d24f546913b956ac2ac7bc0affe6382a2aca633
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
OpenAccessLink http://journals.scholarsportal.info/openUrl.xqy?doi=10.1186/s13046-018-0821-4
PMID 30012200
PQID 2071541745
PQPubID 105475
PageCount 11
ParticipantIDs doaj_primary_oai_doaj_org_article_59b98db4ef614ff5aef5ab80fe82461c
pubmedcentral_primary_oai_pubmedcentral_nih_gov_6048856
proquest_miscellaneous_2071571890
proquest_journals_2071541745
gale_infotracmisc_A547059518
gale_infotracacademiconefile_A547059518
gale_healthsolutions_A547059518
pubmed_primary_30012200
crossref_primary_10_1186_s13046_018_0821_4
crossref_citationtrail_10_1186_s13046_018_0821_4
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2018-07-16
PublicationDateYYYYMMDD 2018-07-16
PublicationDate_xml – month: 07
  year: 2018
  text: 2018-07-16
  day: 16
PublicationDecade 2010
PublicationPlace England
PublicationPlace_xml – name: England
– name: London
PublicationTitle Journal of experimental & clinical cancer research
PublicationTitleAlternate J Exp Clin Cancer Res
PublicationYear 2018
Publisher BioMed Central Ltd
BioMed Central
BMC
Publisher_xml – name: BioMed Central Ltd
– name: BioMed Central
– name: BMC
References N Carlomagno (821_CR8) 2017; 2017
J Wang (821_CR26) 2017; 19
Y Zhen (821_CR32) 2017; 36
G Di Leva (821_CR9) 2014; 9
D Gearing (821_CR17) 1991; 10
Y Peng (821_CR33) 2016; 7
Y Wang (821_CR27) 2017; 27
E Van Cutsem (821_CR1) 2016; 388
M Wang (821_CR6) 2014; 110
M Shah (821_CR2) 2015; 33
J Zhao (821_CR23) 2016; 142
J Shao (821_CR36) 2013; 15
Y Zhang (821_CR35) 2007; 7
H Mirzaei (821_CR5) 2016; 23
A Kosfeld (821_CR30) 2017; 26
A Wagner (821_CR4) 2006; 24
J Wolf (821_CR29) 2016; 291
Q Luo (821_CR31) 2015; 36
D Ma (821_CR14) 2017; 408
H Zeng (821_CR20) 2016; 30
S Tavazoie (821_CR25) 2008; 451
H Sui (821_CR34) 2014; 13
D Bartel (821_CR10) 2004; 116
G Johnson (821_CR38) 2007; 1773
L Cui (821_CR7) 2013; 119
N Martinez (821_CR13) 2009; 31
X Zhang (821_CR16) 2016; 35
F Blanchard (821_CR21) 2003; 38
Y Okamura (821_CR22) 2010; 289
821_CR18
H Zhao (821_CR24) 2015; 47
J Wang (821_CR3) 2012; 21
A Hergovich (821_CR19) 2012; 14
M Zhao (821_CR40) 2016; 7
D Chen (821_CR28) 2012; 18
M Gustems (821_CR39) 2014; 42
C Liu (821_CR15) 2017; 50
J Li (821_CR11) 2014; 43
J Song (821_CR12) 2012; 143
M Gokulnath (821_CR37) 2017; 94
References_xml – volume: 21
  start-page: 119
  issue: 2
  year: 2012
  ident: 821_CR3
  publication-title: Surg Oncol
  doi: 10.1016/j.suronc.2010.12.004
– volume: 14
  start-page: 326
  issue: 6
  year: 2012
  ident: 821_CR19
  publication-title: Breast Cancer Res
  doi: 10.1186/bcr3349
– volume: 142
  start-page: 601
  issue: 3
  year: 2016
  ident: 821_CR23
  publication-title: J Cancer Res Clin Oncol
  doi: 10.1007/s00432-015-2071-6
– volume: 36
  start-page: 1201
  issue: 10
  year: 2015
  ident: 821_CR31
  publication-title: Carcinogenesis
  doi: 10.1093/carcin/bgv108
– volume: 291
  start-page: 16186
  issue: 31
  year: 2016
  ident: 821_CR29
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M116.718551
– volume: 2017
  start-page: 7869802
  year: 2017
  ident: 821_CR8
  publication-title: Biomed Res Int
  doi: 10.1155/2017/7869802
– volume: 1773
  start-page: 1341
  issue: 8
  year: 2007
  ident: 821_CR38
  publication-title: Biochim Biophys Acta
  doi: 10.1016/j.bbamcr.2006.12.009
– volume: 19
  start-page: 72
  issue: 1
  year: 2017
  ident: 821_CR26
  publication-title: Breast Cancer Res
  doi: 10.1186/s13058-017-0865-y
– volume: 15
  start-page: 1075
  issue: 9
  year: 2013
  ident: 821_CR36
  publication-title: Neoplasia
  doi: 10.1593/neo.13966
– volume: 408
  start-page: 23
  year: 2017
  ident: 821_CR14
  publication-title: Cancer Lett
  doi: 10.1016/j.canlet.2017.08.017
– volume: 289
  start-page: 170
  issue: 2
  year: 2010
  ident: 821_CR22
  publication-title: Cancer Lett
  doi: 10.1016/j.canlet.2009.08.013
– volume: 116
  start-page: 281
  issue: 2
  year: 2004
  ident: 821_CR10
  publication-title: Cell
  doi: 10.1016/S0092-8674(04)00045-5
– volume: 143
  start-page: 35
  issue: 1
  year: 2012
  ident: 821_CR12
  publication-title: Gastroenterology
  doi: 10.1053/j.gastro.2012.05.003
– volume: 451
  start-page: 147
  issue: 7175
  year: 2008
  ident: 821_CR25
  publication-title: Nature
  doi: 10.1038/nature06487
– volume: 31
  start-page: 435
  issue: 4
  year: 2009
  ident: 821_CR13
  publication-title: Bioessays
  doi: 10.1002/bies.200800212
– volume: 10
  start-page: 2839
  issue: 10
  year: 1991
  ident: 821_CR17
  publication-title: EMBO J
  doi: 10.1002/j.1460-2075.1991.tb07833.x
– volume: 38
  start-page: 1516
  issue: 6
  year: 2003
  ident: 821_CR21
  publication-title: Hepatology
  doi: 10.1016/j.hep.2003.09.029
– volume: 7
  start-page: e2480
  issue: 11
  year: 2016
  ident: 821_CR33
  publication-title: Cell Death Dis
  doi: 10.1038/cddis.2016.225
– volume: 50
  start-page: 2079
  issue: 6
  year: 2017
  ident: 821_CR15
  publication-title: Int J Oncol
  doi: 10.3892/ijo.2017.3967
– volume: 33
  start-page: 1760
  issue: 16
  year: 2015
  ident: 821_CR2
  publication-title: J Clin Oncol
  doi: 10.1200/JCO.2014.60.1799
– volume: 24
  start-page: 2903
  issue: 18
  year: 2006
  ident: 821_CR4
  publication-title: J Clin Oncol
  doi: 10.1200/JCO.2005.05.0245
– volume: 119
  start-page: 1618
  issue: 9
  year: 2013
  ident: 821_CR7
  publication-title: Cancer
  doi: 10.1002/cncr.27903
– volume: 110
  start-page: 1199
  issue: 5
  year: 2014
  ident: 821_CR6
  publication-title: Br J Cancer
  doi: 10.1038/bjc.2014.14
– volume: 42
  start-page: 3059
  issue: 5
  year: 2014
  ident: 821_CR39
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/gkt1323
– volume: 26
  start-page: 1716
  issue: 9
  year: 2017
  ident: 821_CR30
  publication-title: Hum Mol Genet
  doi: 10.1093/hmg/ddx086
– volume: 43
  start-page: 506
  issue: 2
  year: 2014
  ident: 821_CR11
  publication-title: Chem Soc Rev
  doi: 10.1039/C3CS60312A
– volume: 7
  start-page: 145
  year: 2007
  ident: 821_CR35
  publication-title: BMC Cancer
  doi: 10.1186/1471-2407-7-145
– volume: 35
  start-page: 176
  issue: 1
  year: 2016
  ident: 821_CR16
  publication-title: J Exp Clin Cancer Res
  doi: 10.1186/s13046-016-0452-6
– volume: 30
  start-page: 459
  issue: 3
  year: 2016
  ident: 821_CR20
  publication-title: Cancer Cell
  doi: 10.1016/j.ccell.2016.08.001
– volume: 36
  start-page: 275
  issue: 2
  year: 2017
  ident: 821_CR32
  publication-title: Oncogene
  doi: 10.1038/onc.2016.201
– volume: 9
  start-page: 287
  year: 2014
  ident: 821_CR9
  publication-title: Annu Rev Pathol
  doi: 10.1146/annurev-pathol-012513-104715
– volume: 388
  start-page: 2654
  issue: 10060
  year: 2016
  ident: 821_CR1
  publication-title: Lancet
  doi: 10.1016/S0140-6736(16)30354-3
– volume: 23
  start-page: 4135
  issue: 36
  year: 2016
  ident: 821_CR5
  publication-title: Curr Med Chem
  doi: 10.2174/0929867323666160818093854
– ident: 821_CR18
  doi: 10.1038/nm.2940
– volume: 47
  start-page: 429
  issue: 2
  year: 2015
  ident: 821_CR24
  publication-title: Int J Oncol
  doi: 10.3892/ijo.2015.3052
– volume: 7
  year: 2016
  ident: 821_CR40
  publication-title: Nat Commun
  doi: 10.1038/ncomms11309
– volume: 27
  start-page: 1112
  issue: 7
  year: 2017
  ident: 821_CR27
  publication-title: Genome Res
  doi: 10.1101/gr.219741.116
– volume: 94
  start-page: 370
  issue: Pt A
  year: 2017
  ident: 821_CR37
  publication-title: Int J Biol Macromol
  doi: 10.1016/j.ijbiomac.2016.10.026
– volume: 18
  start-page: 1511
  issue: 10
  year: 2012
  ident: 821_CR28
  publication-title: Nat Med
  doi: 10.1038/nm.2940
– volume: 13
  start-page: 3137
  issue: 12
  year: 2014
  ident: 821_CR34
  publication-title: Mol Cancer Ther
  doi: 10.1158/1535-7163.MCT-14-0167
SSID ssj0061919
Score 2.4110498
Snippet As novel biomarkers for various cancers, microRNAs negatively regulate genes expression via promoting mRNA degradation and suppressing mRNA translation....
Background As novel biomarkers for various cancers, microRNAs negatively regulate genes expression via promoting mRNA degradation and suppressing mRNA...
LIFR has been identified as a metastasis suppressor of breast cancer via the HIPPO-YAP pathway. [...]LIFR expression is down regulated in breast cancer and...
Abstract Background As novel biomarkers for various cancers, microRNAs negatively regulate genes expression via promoting mRNA degradation and suppressing mRNA...
SourceID doaj
pubmedcentral
proquest
gale
pubmed
crossref
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
StartPage 152
SubjectTerms Analysis
Animals
Breast cancer
Cell growth
Cell Line, Tumor
Cytokines
Development and progression
DNA methylation
Experiments
Feedback
Feedback loop
Female
Gastric cancer
Gene expression
Genetic aspects
Health aspects
Humans
Kinases
Laboratories
Leukemia
LIFR
Liver cancer
Male
Medical prognosis
Metastasis
Mice
Mice, Nude
MicroRNA
MicroRNAs
MicroRNAs - metabolism
miR-589
Neoplasm Metastasis
Phosphatidylinositol 3-Kinases - metabolism
Physiological aspects
Proteins
Proto-Oncogene Proteins c-akt - metabolism
Stomach cancer
Stomach Neoplasms - genetics
Stomach Neoplasms - pathology
Tumorigenesis
SummonAdditionalLinks – databaseName: Open Access Journals (DOAJ)
  dbid: DOA
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3LaxQxGA_Sg3gRtT5GWxtBEISwk0wymzlWcWmrFSkWeotJJqnFOrPs49D_vl8eO-wgtBcPe9jNN5D93j-S-X0IvW-crCwUNkKrFgAKZZ5oYzkB57HQPwjmIpfe6ff66JyfXIiLrVFf4U5YogdOipuIxjSyNdx5KCTeC-3gY2TpnQxUaDZkX6h5GzCVcjCgAtrkM0wq68mShgNAgM2BjZnBnkZVKJL1_5uSt2rS-L7kVgGaPUGPc-eID9OOn6IHrnuGHp7ms_Fd9Ovv1RkRssHzeMPOLfGlDkM5LLbBsgusLyO2zukNmxus8bfj2Rn5cVx9nUCzRyw5WXd4kcbT94sb7KG2GW3_4Ou-nz9H57MvPz8fkTw_gVjR0BVxmratp7UEXWkGjanVhnELAK1l3AsAxrQygI-0ZdpOjS219w7ikWn4ruuqeoF2ur5zrxDWgFRaBu0aKyveUg9dI0BLoYUR3EG-LFC50aeymVw8zLi4VhFkyFolEygwgQomULxAH4dH5olZ4y7hT8FIg2AgxY4_gKuo7CrqPlcp0EEwsUpvmA6hrQ4Fn0KXKags0IcoEYIbtm91fkcBlBBoskaSeyNJCEo7Xt64kcpJYakYtHOCAwQUBXo3LIcnw0W3zvXrLAP9QlMW6GXyuuFPV_EctISV6cgfR1oZr3RXvyNleB0Stahf_w81vkGPWIykKaH1HtpZLdZuHzqzlXkbg_AWU1czjQ
  priority: 102
  providerName: Directory of Open Access Journals
– databaseName: Health & Medical Collection
  dbid: 7X7
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1Lb9QwELagSIgL4k1KASMhISFZjZ04jxMqiFVbKEIVlfZmbMdeKtpkye4e-u-ZcbyhEVIPe8h6IiWe1_fZzgwhb2tXZRYSG-NZAwSFC8-0sTkD47GAH6RwoZbeybfi8Cw_nst5XHBbxWOV25gYAnXTWVwjx5UQyPaAn-WH5R-GXaNwdzW20LhN7mDpMrTqcj4SLuAGobEHZMiCIa6Pu5q8KvZXHLcEgUhjfWYBTznJS6F8__9B-lqWmp6gvJaSZg_I_Ygl6cGg_Ifklmsfkbsncbf8Mfl5eX7KZFXTZThz51Z0obFNh6UWdd1TvQhsOwY8aq6opl-PZqfs-1H2ZR_gH7PseNPSfmhY3_VX1EO2M9r-phddt3xCzmaff3w6ZLGjArOy5mvmNG8az4vKu0oLgKpWG5FboGyNyL0EqswzA4xJW6FtaWyqvXfgoULDtS6y7CnZabvWPSdUA3dpBAA4kWZ5wz3gSCCbUksjcwcRNCHpdj6VjeXGsevFhQq0oyrUoAIFKlCoApUn5P14y3KotXGT8EdU0iiIZbLDH12_UNHrlKxNXTUmdx5QiPdSO_iZKoXXxzp6NiGvUcVq-OZ0dHZ1IPMScKfkVULeBQl0d3h8q-NXCzAJWDhrIrk3kQQ3tdPhrRmpGCZW6p9RJ-TNOIx34tG31nWbKAMIok4T8mywuvGls7AzmsJIObHHyaxMR9rzX6GIeIGhWxa7Nz_WC3JPBB8pGS_2yM6637iXgMLW5lVwtb8knyuc
  priority: 102
  providerName: ProQuest
Title miR-589 promotes gastric cancer aggressiveness by a LIFR-PI3K/AKT-c-Jun regulatory feedback loop
URI https://www.ncbi.nlm.nih.gov/pubmed/30012200
https://www.proquest.com/docview/2071541745
https://www.proquest.com/docview/2071571890
https://pubmed.ncbi.nlm.nih.gov/PMC6048856
https://doaj.org/article/59b98db4ef614ff5aef5ab80fe82461c
Volume 37
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1ba9swFBa9wNjL2L3eukyDwWCg1ZYlXx7GaEZD2y2lhAXKXjRJlrKyzM6cBJZ_vyPZMTUrgz3EkOg4sc9F5_si-RyEXucmizUkNhLFBRCUiFoilWYEnEcDfuDU-Fp644vkdMrOr_jVDtq2t2oVuLyV2rl-UtN6_u73r80HCPj3PuCz5GgZueU9IMWu1jKFX9xF-5CYUtfQYMy6RQWgCr7PByTMhDiY3y5y3voVvTTlq_n_PWffSFr9DZU3MtToPrrXQkt83PjCA7RjyofozrhdPH-Evv28nhCe5Xjht-CZJZ5J17VDY-1MX2M58-S7nf-w2mCJP5-NJuTyLP50BGiQaHK-LnHd9K-v6g22kPyU1D_wvKoWj9F0dPLl4ylpGywQzfNoRYyMisJGSWZNJikgVy0VZRoYXEGZ5cCco1gBgZKaSp0qHUprDQQslfBeJnH8BO2VVWkOEJZAZQoKeI6GMSsiC7ASuCeXXHFmYEINULjVp9Bt9XHXBGMuPAvJEtGYQIAJhDOBYAF6252yaEpv_Et46IzUCbqq2f6Dqp6JNggFz1WeFYoZC6DEWi4NvFQWwu27sno6QC-diUXzCGoX--KYsxRgKI-yAL3xEs4f4fK1bB9iACW4Olo9ycOeJESt7g9v3UhsnV5QwHscHJfxAL3qht2Zbidcaap1KwOAIg8D9LTxuu6mY79QGsJI2vPHnlb6I-X1d19TPHEzOU-e_Y_On6O71EdMSqLkEO2t6rV5ARBtpQZoN71KB2h_eHJxORn4PzoGPhjhOBl-_QP7ozav
linkProvider Scholars Portal
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1La9wwEBYhhbaX0nfdpo0KLYWCiC1bXvtQSvpYdrO7oYQE9qZIsrQNTe3tPij7p_obOyN73ZhCbjn4YGsMtmY08316zBDyJrdZbCCwsSgugKBE3DGlTcLAeAzgB8Gtz6U3OU4HZ8nRVEx3yJ_tWRjcVrn1id5RF5XBOXKcCYFoD_hZfJz_Ylg1CldXtyU0arMY2c1voGzLD8MvoN-3nPe_nn4esKaqADMij1bMqqgoXJRmzmaKA1wzSvPEAG0peOIE0MUo1sAalOHK9LQJlXMWrJQruFcpToCCy78FgTdEstebtgQPuIgvJAIROWXII5pV1ChLD5YRLkECccd80Bx6pRMHfbmA_4PClajY3bF5JQT275N7DXalh7WxPSA7tnxIbk-a1flH5PznxQkTWU7nfo-fXdKZwrIghhq0rQVVM8_uGwdL9YYqOh72T9i3YTw6ALjJDDtal3RhZ1hVrFpsqIPoqpX5QS-rav6YnN1IXz8hu2VV2meEKuBKBQfAyMM4KSIHuBXIrVBCi8SCxw5IuO1PaZr05lhl41J6mpOlslaBBBVIVIFMAvK-fWVe5_a4TvgTKqkVxLTc_kG1mMlmlEuR6zwrdGIdoB7nhLJw6SyE38e8fSYg-6hiWZ9xbZ2LPBRJD3CuiLKAvPMS6F7g841qTklAJ2Ciro7kXkcS3ILpNm_NSDZuaSn_DaKAvG6b8U3calfaat3IAGLJw4A8ra2u_enYr8SG0NLr2GOnV7ot5cV3n7Q8xVAh0ufXf9Y-uTM4nYzleHg8ekHucj9eeixK98juarG2LwEBrvQrP-woOb_pcf4XEThqYQ
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=miR-589+promotes+gastric+cancer+aggressiveness+by+a+LIFR-PI3K%2FAKT-c-Jun+regulatory+feedback+loop&rft.jtitle=Journal+of+experimental+%26+clinical+cancer+research&rft.au=Zhang%2C+Feifei&rft.au=Li%2C+Kaitao&rft.au=Pan%2C+Mingxin&rft.au=Li%2C+Weidong&rft.date=2018-07-16&rft.issn=1756-9966&rft.eissn=1756-9966&rft.volume=37&rft.issue=1&rft_id=info:doi/10.1186%2Fs13046-018-0821-4&rft.externalDBID=n%2Fa&rft.externalDocID=10_1186_s13046_018_0821_4
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1756-9966&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1756-9966&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1756-9966&client=summon