Loading…
TGF-β1 Reduces miR-29a Expression to Promote Tumorigenicity and Metastasis of Cholangiocarcinoma by Targeting HDAC4
Transforming growth factor β1 (TGF-β1) and miRNAs play important roles in cholangiocarcinoma progression. In this study, miR-29a level was found significantly decreased in both cholangiocarcinoma tissues and tumor cell lines. TGF-β1 reduced miR-29a expression in tumor cell lines. Furthermore, anti-m...
Saved in:
Published in: | PloS one 2015-10, Vol.10 (10), p.e0136703-e0136703 |
---|---|
Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c4413-dc7ed63beafa2ef993d194bec229c95db48cf6da0d084e265055db5a1de4c2db3 |
---|---|
cites | cdi_FETCH-LOGICAL-c4413-dc7ed63beafa2ef993d194bec229c95db48cf6da0d084e265055db5a1de4c2db3 |
container_end_page | e0136703 |
container_issue | 10 |
container_start_page | e0136703 |
container_title | PloS one |
container_volume | 10 |
creator | Wang, Huiling Li, Caixia Jian, Zhixiang Ou, Yingliang Ou, Jinrui |
description | Transforming growth factor β1 (TGF-β1) and miRNAs play important roles in cholangiocarcinoma progression. In this study, miR-29a level was found significantly decreased in both cholangiocarcinoma tissues and tumor cell lines. TGF-β1 reduced miR-29a expression in tumor cell lines. Furthermore, anti-miR-29a reduced the proliferation and metastasis capacity of cholangiocarcinoma cell lines in vitro, overexpression of miR-29a counteracted TGF-β1-mediated cell growth and metastasis. Subsequent investigation identified HDAC4 is a direct target of miR-29a. In addition, restoration of HDAC4 attenuated miR-29a-mediated inhibition of cell proliferation and metastasis.
TGF-β1/miR-29a/HDAC4 pathway contributes to the pathogenesis of cholangiocarcinoma and our data provide new therapeutic targets for cholangiocarcinoma. |
doi_str_mv | 10.1371/journal.pone.0136703 |
format | article |
fullrecord | <record><control><sourceid>proquest_plos_</sourceid><recordid>TN_cdi_plos_journals_1719376214</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_c0890ce5d0ce4b6789600d7661fc9237</doaj_id><sourcerecordid>3828541491</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4413-dc7ed63beafa2ef993d194bec229c95db48cf6da0d084e265055db5a1de4c2db3</originalsourceid><addsrcrecordid>eNptUt2K1DAYLaK46-obiAa88aZj_ju5EZZx_2BFWcbrkCZfuxnaZkxacV7LB_GZzDjdZVeEkIQv55yc7-MUxWuCF4RV5MMmTHEw3WIbBlhgwmSF2ZPimChGS0kxe_rgflS8SGmDsWBLKZ8XR1RyThgjx8W4vjgvf_8i6AbcZCGh3t-UVBl09nMbISUfBjQG9DWGPoyA1lMfom9h8NaPO2QGhz7DaFJePqHQoNVt6MzQ-mBNtH4IvUH1Dq1NbGH0Q4suP52u-MviWWO6BK_m86T4dn62Xl2W118urlan16Xd2yudrcBJVoNpDIVGKeaI4jVYSpVVwtV8aRvpDHZ4yYFKgUUuCkMccEtdzU6KtwfdbReSngeWNKnyYCpJCc-IqwPCBbPR2-h7E3c6GK__FkJstYmjtx1oi5cKWxAub7yW1VJJjF0lJWmsoqzKWh_n36a6B2dhGKPpHok-fhn8rW7DD82FEoSLLPB-Fojh-wRp1L1PFro8UAjT3jfFXBApVIa--wf6_-74AWVjSClCc2-GYL0P0R1L70Ok5xBl2puHjdyT7lLD_gADIcaj</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1719376214</pqid></control><display><type>article</type><title>TGF-β1 Reduces miR-29a Expression to Promote Tumorigenicity and Metastasis of Cholangiocarcinoma by Targeting HDAC4</title><source>Publicly Available Content Database</source><source>PubMed Central</source><creator>Wang, Huiling ; Li, Caixia ; Jian, Zhixiang ; Ou, Yingliang ; Ou, Jinrui</creator><contributor>Cheng, Jin Q.</contributor><creatorcontrib>Wang, Huiling ; Li, Caixia ; Jian, Zhixiang ; Ou, Yingliang ; Ou, Jinrui ; Cheng, Jin Q.</creatorcontrib><description>Transforming growth factor β1 (TGF-β1) and miRNAs play important roles in cholangiocarcinoma progression. In this study, miR-29a level was found significantly decreased in both cholangiocarcinoma tissues and tumor cell lines. TGF-β1 reduced miR-29a expression in tumor cell lines. Furthermore, anti-miR-29a reduced the proliferation and metastasis capacity of cholangiocarcinoma cell lines in vitro, overexpression of miR-29a counteracted TGF-β1-mediated cell growth and metastasis. Subsequent investigation identified HDAC4 is a direct target of miR-29a. In addition, restoration of HDAC4 attenuated miR-29a-mediated inhibition of cell proliferation and metastasis.
TGF-β1/miR-29a/HDAC4 pathway contributes to the pathogenesis of cholangiocarcinoma and our data provide new therapeutic targets for cholangiocarcinoma.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0136703</identifier><identifier>PMID: 26441331</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Apoptosis ; Biotechnology ; Blotting, Western ; Cancer therapies ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Movement - physiology ; Cell proliferation ; Cell Proliferation - genetics ; Cell Proliferation - physiology ; Cholangiocarcinoma ; Cholangiocarcinoma - genetics ; Cholangiocarcinoma - metabolism ; Cholangiocarcinoma - pathology ; Gene expression ; Histone Deacetylases - genetics ; Histone Deacetylases - metabolism ; Hospitals ; Humans ; Leukemia ; Metastases ; Metastasis ; MicroRNAs ; MicroRNAs - genetics ; Neoplasm Metastasis - genetics ; Pathogenesis ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Restoration ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction - drug effects ; Surgery ; Therapeutic applications ; Transforming Growth Factor beta1 - metabolism ; Transforming Growth Factor beta1 - pharmacology ; Transforming growth factor-b1 ; Tumor cell lines ; Tumorigenicity ; Tumors ; Wound healing</subject><ispartof>PloS one, 2015-10, Vol.10 (10), p.e0136703-e0136703</ispartof><rights>2015 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Wang et al 2015 Wang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4413-dc7ed63beafa2ef993d194bec229c95db48cf6da0d084e265055db5a1de4c2db3</citedby><cites>FETCH-LOGICAL-c4413-dc7ed63beafa2ef993d194bec229c95db48cf6da0d084e265055db5a1de4c2db3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1719376214/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1719376214?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26441331$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Cheng, Jin Q.</contributor><creatorcontrib>Wang, Huiling</creatorcontrib><creatorcontrib>Li, Caixia</creatorcontrib><creatorcontrib>Jian, Zhixiang</creatorcontrib><creatorcontrib>Ou, Yingliang</creatorcontrib><creatorcontrib>Ou, Jinrui</creatorcontrib><title>TGF-β1 Reduces miR-29a Expression to Promote Tumorigenicity and Metastasis of Cholangiocarcinoma by Targeting HDAC4</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Transforming growth factor β1 (TGF-β1) and miRNAs play important roles in cholangiocarcinoma progression. In this study, miR-29a level was found significantly decreased in both cholangiocarcinoma tissues and tumor cell lines. TGF-β1 reduced miR-29a expression in tumor cell lines. Furthermore, anti-miR-29a reduced the proliferation and metastasis capacity of cholangiocarcinoma cell lines in vitro, overexpression of miR-29a counteracted TGF-β1-mediated cell growth and metastasis. Subsequent investigation identified HDAC4 is a direct target of miR-29a. In addition, restoration of HDAC4 attenuated miR-29a-mediated inhibition of cell proliferation and metastasis.
TGF-β1/miR-29a/HDAC4 pathway contributes to the pathogenesis of cholangiocarcinoma and our data provide new therapeutic targets for cholangiocarcinoma.</description><subject>Apoptosis</subject><subject>Biotechnology</subject><subject>Blotting, Western</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Movement - physiology</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Cell Proliferation - physiology</subject><subject>Cholangiocarcinoma</subject><subject>Cholangiocarcinoma - genetics</subject><subject>Cholangiocarcinoma - metabolism</subject><subject>Cholangiocarcinoma - pathology</subject><subject>Gene expression</subject><subject>Histone Deacetylases - genetics</subject><subject>Histone Deacetylases - metabolism</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Leukemia</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>Neoplasm Metastasis - genetics</subject><subject>Pathogenesis</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Restoration</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Signal Transduction - drug effects</subject><subject>Surgery</subject><subject>Therapeutic applications</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Transforming Growth Factor beta1 - pharmacology</subject><subject>Transforming growth factor-b1</subject><subject>Tumor cell lines</subject><subject>Tumorigenicity</subject><subject>Tumors</subject><subject>Wound healing</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUt2K1DAYLaK46-obiAa88aZj_ju5EZZx_2BFWcbrkCZfuxnaZkxacV7LB_GZzDjdZVeEkIQv55yc7-MUxWuCF4RV5MMmTHEw3WIbBlhgwmSF2ZPimChGS0kxe_rgflS8SGmDsWBLKZ8XR1RyThgjx8W4vjgvf_8i6AbcZCGh3t-UVBl09nMbISUfBjQG9DWGPoyA1lMfom9h8NaPO2QGhz7DaFJePqHQoNVt6MzQ-mBNtH4IvUH1Dq1NbGH0Q4suP52u-MviWWO6BK_m86T4dn62Xl2W118urlan16Xd2yudrcBJVoNpDIVGKeaI4jVYSpVVwtV8aRvpDHZ4yYFKgUUuCkMccEtdzU6KtwfdbReSngeWNKnyYCpJCc-IqwPCBbPR2-h7E3c6GK__FkJstYmjtx1oi5cKWxAub7yW1VJJjF0lJWmsoqzKWh_n36a6B2dhGKPpHok-fhn8rW7DD82FEoSLLPB-Fojh-wRp1L1PFro8UAjT3jfFXBApVIa--wf6_-74AWVjSClCc2-GYL0P0R1L70Ok5xBl2puHjdyT7lLD_gADIcaj</recordid><startdate>20151006</startdate><enddate>20151006</enddate><creator>Wang, Huiling</creator><creator>Li, Caixia</creator><creator>Jian, Zhixiang</creator><creator>Ou, Yingliang</creator><creator>Ou, Jinrui</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20151006</creationdate><title>TGF-β1 Reduces miR-29a Expression to Promote Tumorigenicity and Metastasis of Cholangiocarcinoma by Targeting HDAC4</title><author>Wang, Huiling ; Li, Caixia ; Jian, Zhixiang ; Ou, Yingliang ; Ou, Jinrui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4413-dc7ed63beafa2ef993d194bec229c95db48cf6da0d084e265055db5a1de4c2db3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Apoptosis</topic><topic>Biotechnology</topic><topic>Blotting, Western</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Movement - physiology</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Cell Proliferation - physiology</topic><topic>Cholangiocarcinoma</topic><topic>Cholangiocarcinoma - genetics</topic><topic>Cholangiocarcinoma - metabolism</topic><topic>Cholangiocarcinoma - pathology</topic><topic>Gene expression</topic><topic>Histone Deacetylases - genetics</topic><topic>Histone Deacetylases - metabolism</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Leukemia</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>Neoplasm Metastasis - genetics</topic><topic>Pathogenesis</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>Restoration</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Signal Transduction - drug effects</topic><topic>Surgery</topic><topic>Therapeutic applications</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>Transforming Growth Factor beta1 - pharmacology</topic><topic>Transforming growth factor-b1</topic><topic>Tumor cell lines</topic><topic>Tumorigenicity</topic><topic>Tumors</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Huiling</creatorcontrib><creatorcontrib>Li, Caixia</creatorcontrib><creatorcontrib>Jian, Zhixiang</creatorcontrib><creatorcontrib>Ou, Yingliang</creatorcontrib><creatorcontrib>Ou, Jinrui</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>ProQuest Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>Advanced Technologies & Aerospace Database (1962 - current)</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>https://resources.nclive.org/materials</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agriculture Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>ProQuest Biological Science Journals</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest advanced technologies & aerospace journals</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials science collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Huiling</au><au>Li, Caixia</au><au>Jian, Zhixiang</au><au>Ou, Yingliang</au><au>Ou, Jinrui</au><au>Cheng, Jin Q.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TGF-β1 Reduces miR-29a Expression to Promote Tumorigenicity and Metastasis of Cholangiocarcinoma by Targeting HDAC4</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-10-06</date><risdate>2015</risdate><volume>10</volume><issue>10</issue><spage>e0136703</spage><epage>e0136703</epage><pages>e0136703-e0136703</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Transforming growth factor β1 (TGF-β1) and miRNAs play important roles in cholangiocarcinoma progression. In this study, miR-29a level was found significantly decreased in both cholangiocarcinoma tissues and tumor cell lines. TGF-β1 reduced miR-29a expression in tumor cell lines. Furthermore, anti-miR-29a reduced the proliferation and metastasis capacity of cholangiocarcinoma cell lines in vitro, overexpression of miR-29a counteracted TGF-β1-mediated cell growth and metastasis. Subsequent investigation identified HDAC4 is a direct target of miR-29a. In addition, restoration of HDAC4 attenuated miR-29a-mediated inhibition of cell proliferation and metastasis.
TGF-β1/miR-29a/HDAC4 pathway contributes to the pathogenesis of cholangiocarcinoma and our data provide new therapeutic targets for cholangiocarcinoma.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26441331</pmid><doi>10.1371/journal.pone.0136703</doi><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1932-6203 |
ispartof | PloS one, 2015-10, Vol.10 (10), p.e0136703-e0136703 |
issn | 1932-6203 1932-6203 |
language | eng |
recordid | cdi_plos_journals_1719376214 |
source | Publicly Available Content Database; PubMed Central |
subjects | Apoptosis Biotechnology Blotting, Western Cancer therapies Cell cycle Cell growth Cell Line, Tumor Cell Movement - genetics Cell Movement - physiology Cell proliferation Cell Proliferation - genetics Cell Proliferation - physiology Cholangiocarcinoma Cholangiocarcinoma - genetics Cholangiocarcinoma - metabolism Cholangiocarcinoma - pathology Gene expression Histone Deacetylases - genetics Histone Deacetylases - metabolism Hospitals Humans Leukemia Metastases Metastasis MicroRNAs MicroRNAs - genetics Neoplasm Metastasis - genetics Pathogenesis Repressor Proteins - genetics Repressor Proteins - metabolism Restoration Reverse Transcriptase Polymerase Chain Reaction Signal Transduction - drug effects Surgery Therapeutic applications Transforming Growth Factor beta1 - metabolism Transforming Growth Factor beta1 - pharmacology Transforming growth factor-b1 Tumor cell lines Tumorigenicity Tumors Wound healing |
title | TGF-β1 Reduces miR-29a Expression to Promote Tumorigenicity and Metastasis of Cholangiocarcinoma by Targeting HDAC4 |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T11%3A37%3A15IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=TGF-%CE%B21%20Reduces%20miR-29a%20Expression%20to%20Promote%20Tumorigenicity%20and%20Metastasis%20of%20Cholangiocarcinoma%20by%20Targeting%20HDAC4&rft.jtitle=PloS%20one&rft.au=Wang,%20Huiling&rft.date=2015-10-06&rft.volume=10&rft.issue=10&rft.spage=e0136703&rft.epage=e0136703&rft.pages=e0136703-e0136703&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0136703&rft_dat=%3Cproquest_plos_%3E3828541491%3C/proquest_plos_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c4413-dc7ed63beafa2ef993d194bec229c95db48cf6da0d084e265055db5a1de4c2db3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1719376214&rft_id=info:pmid/26441331&rfr_iscdi=true |