Exosomal long non-coding RNA-LINC00839 promotes lung adenocarcinoma progression by activating NF-κB signaling pathway
Lung adenocarcinoma is the most common type of lung cancer, accounting for approximately 40% of all lung cancer cases, and has the highest incidence among lung cancer subtypes. Recent studies have suggested that long non-coding RNAs (lncRNAs) play a crucial role in the initiation and progression of...
Saved in:
Published in | Annals of medicine (Helsinki) Vol. 56; no. 1; p. 2430029 |
---|---|
Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Taylor & Francis
01.12.2024
Taylor & Francis Group |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | Lung adenocarcinoma is the most common type of lung cancer, accounting for approximately 40% of all lung cancer cases, and has the highest incidence among lung cancer subtypes. Recent studies have suggested that long non-coding RNAs (lncRNAs) play a crucial role in the initiation and progression of lung adenocarcinoma.
Based on integrative analysis through databases, we screened Long intergenic non-protein coding RNA 00839 (LINC00839) as one of the most highly upregulated lncRNAs in lung adenocarcinoma.
and
experiments demonstrated that LINC00839 promotes lung adenocarcinoma proliferation, migration, and invasion and that it is present in exosomes secreted by lung adenocarcinoma cells.
In the cytoplasm, LINC00839 regulates the Toll-like receptor 4 (TLR4)/NF-κB signaling pathway by acting as a molecular sponge of miR-17-5p, thereby influencing the biological behavior of lung adenocarcinoma cells. LINC00839 binds to Polypyrimidine tract binding protein 1 (PTBP1) in the nucleus to regulate the nuclear translocation of NF-κB p65 molecules and, consequently, the transcription of downstream molecules.
Our study confirmed that LINC00839 promotes the biological progression of lung adenocarcinoma by performing dual roles in the cytoplasm and nucleus to co-regulate the NF-κB signaling pathway. |
---|---|
AbstractList | Lung adenocarcinoma is the most common type of lung cancer, accounting for approximately 40% of all lung cancer cases, and has the highest incidence among lung cancer subtypes. Recent studies have suggested that long non-coding RNAs (lncRNAs) play a crucial role in the initiation and progression of lung adenocarcinoma.
Based on integrative analysis through databases, we screened Long intergenic non-protein coding RNA 00839 (LINC00839) as one of the most highly upregulated lncRNAs in lung adenocarcinoma.
and
experiments demonstrated that LINC00839 promotes lung adenocarcinoma proliferation, migration, and invasion and that it is present in exosomes secreted by lung adenocarcinoma cells.
In the cytoplasm, LINC00839 regulates the Toll-like receptor 4 (TLR4)/NF-κB signaling pathway by acting as a molecular sponge of miR-17-5p, thereby influencing the biological behavior of lung adenocarcinoma cells. LINC00839 binds to Polypyrimidine tract binding protein 1 (PTBP1) in the nucleus to regulate the nuclear translocation of NF-κB p65 molecules and, consequently, the transcription of downstream molecules.
Our study confirmed that LINC00839 promotes the biological progression of lung adenocarcinoma by performing dual roles in the cytoplasm and nucleus to co-regulate the NF-κB signaling pathway. Lung adenocarcinoma is the most common type of lung cancer, accounting for approximately 40% of all lung cancer cases, and has the highest incidence among lung cancer subtypes. Recent studies have suggested that long non-coding RNAs (lncRNAs) play a crucial role in the initiation and progression of lung adenocarcinoma.BACKGROUNDLung adenocarcinoma is the most common type of lung cancer, accounting for approximately 40% of all lung cancer cases, and has the highest incidence among lung cancer subtypes. Recent studies have suggested that long non-coding RNAs (lncRNAs) play a crucial role in the initiation and progression of lung adenocarcinoma.Based on integrative analysis through databases, we screened Long intergenic non-protein coding RNA 00839 (LINC00839) as one of the most highly upregulated lncRNAs in lung adenocarcinoma. In vitro and in vivo experiments demonstrated that LINC00839 promotes lung adenocarcinoma proliferation, migration, and invasion and that it is present in exosomes secreted by lung adenocarcinoma cells.METHODSBased on integrative analysis through databases, we screened Long intergenic non-protein coding RNA 00839 (LINC00839) as one of the most highly upregulated lncRNAs in lung adenocarcinoma. In vitro and in vivo experiments demonstrated that LINC00839 promotes lung adenocarcinoma proliferation, migration, and invasion and that it is present in exosomes secreted by lung adenocarcinoma cells.In the cytoplasm, LINC00839 regulates the Toll-like receptor 4 (TLR4)/NF-κB signaling pathway by acting as a molecular sponge of miR-17-5p, thereby influencing the biological behavior of lung adenocarcinoma cells. LINC00839 binds to Polypyrimidine tract binding protein 1 (PTBP1) in the nucleus to regulate the nuclear translocation of NF-κB p65 molecules and, consequently, the transcription of downstream molecules.RESULTSIn the cytoplasm, LINC00839 regulates the Toll-like receptor 4 (TLR4)/NF-κB signaling pathway by acting as a molecular sponge of miR-17-5p, thereby influencing the biological behavior of lung adenocarcinoma cells. LINC00839 binds to Polypyrimidine tract binding protein 1 (PTBP1) in the nucleus to regulate the nuclear translocation of NF-κB p65 molecules and, consequently, the transcription of downstream molecules.Our study confirmed that LINC00839 promotes the biological progression of lung adenocarcinoma by performing dual roles in the cytoplasm and nucleus to co-regulate the NF-κB signaling pathway.CONCLUSIONSOur study confirmed that LINC00839 promotes the biological progression of lung adenocarcinoma by performing dual roles in the cytoplasm and nucleus to co-regulate the NF-κB signaling pathway. Background Lung adenocarcinoma is the most common type of lung cancer, accounting for approximately 40% of all lung cancer cases, and has the highest incidence among lung cancer subtypes. Recent studies have suggested that long non-coding RNAs (lncRNAs) play a crucial role in the initiation and progression of lung adenocarcinoma.Methods Based on integrative analysis through databases, we screened Long intergenic non-protein coding RNA 00839 (LINC00839) as one of the most highly upregulated lncRNAs in lung adenocarcinoma. In vitro and in vivo experiments demonstrated that LINC00839 promotes lung adenocarcinoma proliferation, migration, and invasion and that it is present in exosomes secreted by lung adenocarcinoma cells.Results In the cytoplasm, LINC00839 regulates the Toll-like receptor 4 (TLR4)/NF-κB signaling pathway by acting as a molecular sponge of miR-17-5p, thereby influencing the biological behavior of lung adenocarcinoma cells. LINC00839 binds to Polypyrimidine tract binding protein 1 (PTBP1) in the nucleus to regulate the nuclear translocation of NF-κB p65 molecules and, consequently, the transcription of downstream molecules.Conclusions Our study confirmed that LINC00839 promotes the biological progression of lung adenocarcinoma by performing dual roles in the cytoplasm and nucleus to co-regulate the NF-κB signaling pathway. |
Author | Hu, Jing Wang, Hongyi Wang, Feiran Sun, Yue Zhen, Fang Liang, Xiao Wang, Yaru |
Author_xml | – sequence: 1 givenname: Yue surname: Sun fullname: Sun, Yue organization: Department of Breast Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China – sequence: 2 givenname: Fang surname: Zhen fullname: Zhen, Fang organization: Department of Breast Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China – sequence: 3 givenname: Hongyi surname: Wang fullname: Wang, Hongyi organization: Department of Breast Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China – sequence: 4 givenname: Xiao surname: Liang fullname: Liang, Xiao organization: Key laboratory of Preservation of Human Genetic Resources and Disease Control in China, Harbin Medical University, Ministry of Education, Harbin, China – sequence: 5 givenname: Yaru surname: Wang fullname: Wang, Yaru organization: Department of Breast Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China – sequence: 6 givenname: Feiran surname: Wang fullname: Wang, Feiran organization: Department of Breast Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China – sequence: 7 givenname: Jing orcidid: 0000-0001-7922-6026 surname: Hu fullname: Hu, Jing organization: Department of Breast Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China, Key laboratory of Preservation of Human Genetic Resources and Disease Control in China, Harbin Medical University, Ministry of Education, Harbin, China |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/39582330$$D View this record in MEDLINE/PubMed |
BookMark | eNqFks-O0zAQxi20iO0uPAIoRy4p4z9JbHFAS7ULlaoiIThbE8fJepXGxU4LfTUegmfCod0Vy4WTrZnf981I812Qs8EPlpCXFOYUJLyBShZcKpgzYGLOBAdg6gmZUV4WOYMSzshsYvIJOicXMd5BQioKz8g5V4VknMOM7K9_-Og32Ge9H7osDcmNb1z6fl5f5avlegEgucq2wW_8aGPW71IPGzt4g8G4IWmnZhdsjM4PWX3I0Ixuj-Nksr7Jf_18n0XXDdhPhS2Ot9_x8Jw8bbGP9sXpvSRfb66_LD7mq08flourVW5EJcfccgUtUGEaLpoWKsZVY6RsSgtFZVtbKSylNIgKDTLDeNVYBrWqhRFCWcYvyfLo23i809vgNhgO2qPTfwo-dBrD6ExvtVW2VXXDkZWtqEypKpDIQbQCyprzMnm9O3ptd_XGNsYOY8D-kenjzuBudef3mtJCAZUyObw-OQT_bWfjqDcuGtv3OFi_i5pTzkooFRUJffX3sIcp95dLQHEETPAxBts-IBT0lBB9nxA9JUSfEpJ0b__RGTemY_lpZ9f_R_0b9vTBeQ |
CitedBy_id | crossref_primary_10_3389_fphar_2025_1485661 |
Cites_doi | 10.1038/onc.2017.184 10.1016/j.ijbiomac.2018.10.142 10.1007/s11064-022-03613-0 10.1038/nm.4424 10.1042/BCJ20170280 10.15252/embr.202154128 10.1111/joim.12019 10.1038/s41580-020-00315-9 10.1093/nar/gkv489 10.1042/BST20191059 10.1016/j.yexcr.2021.112834 10.1016/S0140-6736(16)30958-8 10.1038/s41418-021-00888-8 10.1007/s00018-016-2174-5 10.1186/s13287-022-03037-1 10.1093/nar/gkx247 10.1186/s13045-020-00951-w 10.1631/jzus.B1900422 10.1002/wrna.1413 10.1126/science.aau6977 10.1038/s41419-022-04509-1 10.1111/cas.14555 10.7150/thno.71100 10.1016/j.cell.2013.02.012 10.1016/bs.mie.2014.10.050 10.7150/thno.34126 10.1038/nri910 10.1158/0008-5472.CAN-19-0799 10.1186/s12943-019-1122-z 10.1002/ijc.25704 10.1038/s41598-022-16972-z 10.1016/j.molcel.2012.09.028 10.1016/j.jaci.2017.08.034 10.7150/thno.59546 10.1186/s12943-018-0836-7 10.7150/ijbs.57338 10.1371/journal.pone.0158708 10.1186/s12943-019-1109-9 10.1038/s41392-020-00450-x 10.1038/ni.2065 10.1111/cpr.13168 10.1038/s41392-020-00312-6 10.1007/s10456-017-9562-9 10.1093/nar/gkw104 10.3892/or.2018.6652 |
ContentType | Journal Article |
Copyright | 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group 2024 The Author(s) |
Copyright_xml | – notice: 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group 2024 The Author(s) |
DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM DOA |
DOI | 10.1080/07853890.2024.2430029 |
DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
DatabaseTitleList | MEDLINE MEDLINE - Academic |
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 |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine |
DocumentTitleAlternate | Y. Sun et al |
EISSN | 1365-2060 |
ExternalDocumentID | oai_doaj_org_article_e9ef9bd3a26f47c69708a304f406b336 PMC11590188 39582330 10_1080_07853890_2024_2430029 |
Genre | Journal Article |
GroupedDBID | --- 00X 03L 0YH 23M 36B 4.4 5GY 5RE AAFWJ AALUX AAYXX ABLKL ABUPF ACGEJ ACGFS ADCVX ADRBQ ADXPE AENEX AEOZL AFKVX AGYJP AIJEM AJWEG ALMA_UNASSIGNED_HOLDINGS BABNJ BLEHA BOHLJ CCCUG CITATION CS3 DKSSO EBD EBS EMB EMOBN F5P GROUPED_DOAJ H13 HZ~ KRBQP KSSTO KWAYT KYCEM LJTGL M4Z O9- OK1 P2P RPM SV3 TDBHL TFDNU TFL TFW V1S WH7 ~1N .55 .GJ 34G 39C 3O- 53G 5VS AALIY AAORF AAPXX ABWCV ABZEW ADFZZ AFFNX AFLEI AJVHN AWYRJ BRMBE CAG CGR COF CUY CVF CYYVM CZDIS DRXRE DWTOO ECM EIF EJD JENTW M44 NPM NUSFT OVD QQXMO TEORI X7M ZGI ZXP 7X8 5PM |
ID | FETCH-LOGICAL-c478t-e390f014cd34df07239dc88d6e057efe79a688caa9aca2c237de20b9b4c449e23 |
IEDL.DBID | DOA |
ISSN | 0785-3890 1365-2060 |
IngestDate | Wed Aug 27 01:29:31 EDT 2025 Thu Aug 21 18:32:03 EDT 2025 Thu Jul 10 18:27:03 EDT 2025 Mon Jul 21 05:55:24 EDT 2025 Thu Apr 24 23:10:38 EDT 2025 Tue Jul 01 01:44:53 EDT 2025 |
IsDoiOpenAccess | true |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 1 |
Keywords | LINC00839 miR-17-5p PTBP1 NF-κB p65 nuclear translocation lung adenocarcinoma |
Language | English |
License | This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent. |
LinkModel | DirectLink |
MergedId | FETCHMERGED-LOGICAL-c478t-e390f014cd34df07239dc88d6e057efe79a688caa9aca2c237de20b9b4c449e23 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Yue Sun, Fang Zhen, Hongyi Wang contributed equally. Supplemental data for this article can be accessed online at https://doi.org/10.1080/07853890.2024.2430029. |
ORCID | 0000-0001-7922-6026 |
OpenAccessLink | https://doaj.org/article/e9ef9bd3a26f47c69708a304f406b336 |
PMID | 39582330 |
PQID | 3132606914 |
PQPubID | 23479 |
ParticipantIDs | doaj_primary_oai_doaj_org_article_e9ef9bd3a26f47c69708a304f406b336 pubmedcentral_primary_oai_pubmedcentral_nih_gov_11590188 proquest_miscellaneous_3132606914 pubmed_primary_39582330 crossref_primary_10_1080_07853890_2024_2430029 crossref_citationtrail_10_1080_07853890_2024_2430029 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 2024-Dec |
PublicationDateYYYYMMDD | 2024-12-01 |
PublicationDate_xml | – month: 12 year: 2024 text: 2024-Dec |
PublicationDecade | 2020 |
PublicationPlace | England |
PublicationPlace_xml | – name: England |
PublicationTitle | Annals of medicine (Helsinki) |
PublicationTitleAlternate | Ann Med |
PublicationYear | 2024 |
Publisher | Taylor & Francis Taylor & Francis Group |
Publisher_xml | – name: Taylor & Francis – name: Taylor & Francis Group |
References | e_1_3_6_30_1 e_1_3_6_31_1 e_1_3_6_32_1 e_1_3_6_33_1 e_1_3_6_11_1 e_1_3_6_10_1 e_1_3_6_15_1 e_1_3_6_38_1 e_1_3_6_14_1 e_1_3_6_39_1 e_1_3_6_13_1 e_1_3_6_12_1 e_1_3_6_19_1 e_1_3_6_34_1 e_1_3_6_18_1 e_1_3_6_35_1 e_1_3_6_17_1 e_1_3_6_36_1 e_1_3_6_16_1 e_1_3_6_37_1 e_1_3_6_42_1 e_1_3_6_20_1 e_1_3_6_41_1 e_1_3_6_21_1 e_1_3_6_44_1 e_1_3_6_22_1 e_1_3_6_43_1 e_1_3_6_2_1 e_1_3_6_40_1 e_1_3_6_6_1 e_1_3_6_5_1 e_1_3_6_4_1 e_1_3_6_3_1 e_1_3_6_9_1 e_1_3_6_8_1 e_1_3_6_7_1 e_1_3_6_27_1 e_1_3_6_28_1 e_1_3_6_29_1 e_1_3_6_23_1 e_1_3_6_46_1 e_1_3_6_24_1 e_1_3_6_45_1 e_1_3_6_25_1 e_1_3_6_26_1 |
References_xml | – ident: e_1_3_6_3_1 doi: 10.1038/onc.2017.184 – ident: e_1_3_6_29_1 doi: 10.1016/j.ijbiomac.2018.10.142 – ident: e_1_3_6_35_1 doi: 10.1007/s11064-022-03613-0 – ident: e_1_3_6_31_1 doi: 10.1038/nm.4424 – ident: e_1_3_6_37_1 doi: 10.1042/BCJ20170280 – ident: e_1_3_6_4_1 doi: 10.15252/embr.202154128 – ident: e_1_3_6_21_1 doi: 10.1111/joim.12019 – ident: e_1_3_6_25_1 doi: 10.1038/s41580-020-00315-9 – ident: e_1_3_6_26_1 doi: 10.1093/nar/gkv489 – ident: e_1_3_6_27_1 doi: 10.1042/BST20191059 – ident: e_1_3_6_10_1 doi: 10.1016/j.yexcr.2021.112834 – ident: e_1_3_6_2_1 doi: 10.1016/S0140-6736(16)30958-8 – ident: e_1_3_6_33_1 doi: 10.1038/s41418-021-00888-8 – ident: e_1_3_6_30_1 doi: 10.1007/s00018-016-2174-5 – ident: e_1_3_6_11_1 doi: 10.1186/s13287-022-03037-1 – ident: e_1_3_6_16_1 doi: 10.1093/nar/gkx247 – ident: e_1_3_6_43_1 doi: 10.1186/s13045-020-00951-w – ident: e_1_3_6_6_1 doi: 10.1631/jzus.B1900422 – ident: e_1_3_6_23_1 doi: 10.1002/wrna.1413 – ident: e_1_3_6_22_1 doi: 10.1126/science.aau6977 – ident: e_1_3_6_36_1 doi: 10.1038/s41419-022-04509-1 – ident: e_1_3_6_5_1 doi: 10.1111/cas.14555 – ident: e_1_3_6_8_1 doi: 10.7150/thno.71100 – ident: e_1_3_6_24_1 doi: 10.1016/j.cell.2013.02.012 – ident: e_1_3_6_28_1 doi: 10.1016/bs.mie.2014.10.050 – ident: e_1_3_6_20_1 doi: 10.7150/thno.34126 – ident: e_1_3_6_15_1 doi: 10.1038/nri910 – ident: e_1_3_6_45_1 doi: 10.1158/0008-5472.CAN-19-0799 – ident: e_1_3_6_38_1 doi: 10.1186/s12943-019-1122-z – ident: e_1_3_6_18_1 doi: 10.1002/ijc.25704 – ident: e_1_3_6_34_1 doi: 10.1038/s41598-022-16972-z – ident: e_1_3_6_40_1 doi: 10.1016/j.molcel.2012.09.028 – ident: e_1_3_6_9_1 doi: 10.1016/j.jaci.2017.08.034 – ident: e_1_3_6_7_1 doi: 10.7150/thno.59546 – ident: e_1_3_6_32_1 doi: 10.1186/s12943-018-0836-7 – ident: e_1_3_6_12_1 doi: 10.7150/ijbs.57338 – ident: e_1_3_6_39_1 doi: 10.1371/journal.pone.0158708 – ident: e_1_3_6_41_1 doi: 10.1186/s12943-019-1109-9 – ident: e_1_3_6_42_1 doi: 10.1038/s41392-020-00450-x – ident: e_1_3_6_14_1 doi: 10.1038/ni.2065 – ident: e_1_3_6_44_1 doi: 10.1111/cpr.13168 – ident: e_1_3_6_13_1 doi: 10.1038/s41392-020-00312-6 – ident: e_1_3_6_19_1 doi: 10.1007/s10456-017-9562-9 – ident: e_1_3_6_46_1 doi: 10.1093/nar/gkw104 – ident: e_1_3_6_17_1 doi: 10.3892/or.2018.6652 |
SSID | ssj0002710 |
Score | 2.4484465 |
Snippet | Lung adenocarcinoma is the most common type of lung cancer, accounting for approximately 40% of all lung cancer cases, and has the highest incidence among lung... Background Lung adenocarcinoma is the most common type of lung cancer, accounting for approximately 40% of all lung cancer cases, and has the highest incidence... |
SourceID | doaj pubmedcentral proquest pubmed crossref |
SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
StartPage | 2430029 |
SubjectTerms | Adenocarcinoma of Lung - genetics Adenocarcinoma of Lung - metabolism Adenocarcinoma of Lung - pathology Animals Cell Line, Tumor Cell Movement - genetics Cell Proliferation - genetics Disease Progression Exosomes - genetics Exosomes - metabolism Gene Expression Regulation, Neoplastic Humans LINC00839 lung adenocarcinoma Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology Mice MicroRNAs - genetics MicroRNAs - metabolism miR-17-5p NF-kappa B - metabolism NF-κB p65 nuclear translocation Oncology PTBP1 RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Signal Transduction - genetics Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - metabolism |
Title | Exosomal long non-coding RNA-LINC00839 promotes lung adenocarcinoma progression by activating NF-κB signaling pathway |
URI | https://www.ncbi.nlm.nih.gov/pubmed/39582330 https://www.proquest.com/docview/3132606914 https://pubmed.ncbi.nlm.nih.gov/PMC11590188 https://doaj.org/article/e9ef9bd3a26f47c69708a304f406b336 |
Volume | 56 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1LT9wwELYqDohLVR4t4SUj9Wqatb2OfWTRrhCCPVRF4hb5Fai03SB2aeGv8SP4Tcw4yYpFSFx6dWzH8Ywz39jjbwj5zrVV0hrLVKUCkwCRGbjNmkVQGG2tcz5x6V2M1emlPLvqX71K9YUxYQ09cDNxP6KJlXFBWK4qWXhlCugDfPAKLJETIpFtg83rnKn2H8yLxEMA9q_PwCTn3d0dZNWGMiwC35DLIy4FHkwtWaVE3v8e4nwbOPnKEo2-kM8thKTHzdDXyac43SCrF-0h-Sb5O3yoZ_UfqDKpp9cU_HvmazRR9Of4mJ2DG4-IyNDbFIkXZ3QCC55a-AGBXbuDPqAtTXFbDWcHdY8Urz_g5i1UHI_Y89OAYuCHxbvsFJMa_7OPW-RyNPx1csra9ArMy0LPWRQmr8BD8kHIUOUFFyZ4rYOKgOFiFQtjldbegiS95Z6LIkSeO-Okl9JELr6SFfiEuE1oEYMJDsCbQG4f6KTnvJDeqyisqfq9jMhuekvfco9jCoxJ2esoSluplCiVspVKRo4WzW4b8o2PGgxQdovKyJ2dCkCjylajyo80KiOHneRLWGt4gGKnsb6flUhzCdpsejIj3xpNWLxKmL7mQuQZ0Us6sjSW5SfT3zeJzxtAOaAyrXf-x-h3yRrOSBNxs0dW5nf3cR9w09wdpCVykDa0XgC-XhIl |
linkProvider | Directory of Open Access Journals |
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=Exosomal+long+non-coding+RNA-LINC00839+promotes+lung+adenocarcinoma+progression+by+activating+NF-%CE%BAB+signaling+pathway&rft.jtitle=Annals+of+medicine+%28Helsinki%29&rft.au=Sun%2C+Yue&rft.au=Zhen%2C+Fang&rft.au=Wang%2C+Hongyi&rft.au=Liang%2C+Xiao&rft.date=2024-12-01&rft.issn=0785-3890&rft.eissn=1365-2060&rft.volume=56&rft.issue=1&rft_id=info:doi/10.1080%2F07853890.2024.2430029&rft.externalDBID=n%2Fa&rft.externalDocID=10_1080_07853890_2024_2430029 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0785-3890&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0785-3890&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0785-3890&client=summon |