MicroRNA-29c mediates initiation of gastric carcinogenesis by directly targeting ITGB1
Objective Gastric cancer (GC) remains difficult to cure due to heterogeneity in a clinical challenge and the molecular mechanisms underlying this disease are complex and not completely understood. Accumulating evidence suggests that microRNAs (miRNAs) play an important role in GC, but the role of sp...
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| Veröffentlicht in: | Gut 2015-02, Vol.64 (2), p.203-214 |
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| creator | Han, Tae-Su Hur, Keun Xu, Guorong Choi, Boram Okugawa, Yoshinaga Toiyama, Yuji Oshima, Hiroko Oshima, Masanobu Lee, Hyuk-Joon Kim, V Narry Chang, Aaron N Goel, Ajay Yang, Han-Kwang |
| description | Objective Gastric cancer (GC) remains difficult to cure due to heterogeneity in a clinical challenge and the molecular mechanisms underlying this disease are complex and not completely understood. Accumulating evidence suggests that microRNAs (miRNAs) play an important role in GC, but the role of specific miRNAs involved in this disease remains elusive. We performed next generation sequencing (NGS)-based whole-transcriptome profiling to discover GC-specific miRNAs, followed by functional validation of results. Design NGS-based miRNA profiles were generated in matched pairs of GCs and adjacent normal mucosa (NM). Quantitative RT-PCR validation of miR-29c expression was performed in 274 gastric tissues, which included two cohorts of matched GC and NM specimens. Functional validation of miR-29c and its gene targets was undertaken in cell lines, as well as K19-C2mE and K19-Wnt1/C2mE transgenic mice. Results NGS analysis revealed four GC-specific miRNAs. Among these, miR-29c expression was significantly decreased in GC versus NM tissues (p |
| doi_str_mv | 10.1136/gutjnl-2013-306640 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4384419</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4014718331</sourcerecordid><originalsourceid>FETCH-LOGICAL-b637t-1a021f9d52754edd7ea1d1b280977ba33c4f8f450d4146acb087ef444c1989063</originalsourceid><addsrcrecordid>eNqNkU1rFTEUhoMo9lr9Ay4k4MZNbL4mHxuhLVoLtQWpbkMmkxlzmZvUJCPcf28uU4t25SqBPOflvHkAeE3we0KYOJmWuo0zopgwxLAQHD8BG8KFQowq9RRsMCYSdZLrI_CilC3GWClNnoMjypXEguIN-P4luJy-Xp8iqh3c-SHY6gsMMdR2CynCNMLJlpqDg85mF2KafPQlFNjv4RCyd3Xew2rz5GuIE7y8vTgjL8Gz0c7Fv7o_j8G3Tx9vzz-jq5uLy_PTK9QLJisiFlMy6qGjsuN-GKS3ZCA9VVhL2VvGHB_VyDs88NbLuh4r6UfOuSNaaSzYMfiw5t4tfVve-Viznc1dDjub9ybZYP59ieGHmdIvw5ninOgW8O4-IKefiy_V7EJxfp5t9GkphiishJJSH9C3j9BtWnJs9QxpABddRw8UXan2raVkPz4sQ7A5aDOrNnPQZlZtbejN3zUeRv54agBagX63_Z_A3wOhoxQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1779465529</pqid></control><display><type>article</type><title>MicroRNA-29c mediates initiation of gastric carcinogenesis by directly targeting ITGB1</title><source>MEDLINE</source><source>BMJ Journals - NESLi2</source><source>PubMed Central</source><creator>Han, Tae-Su ; Hur, Keun ; Xu, Guorong ; Choi, Boram ; Okugawa, Yoshinaga ; Toiyama, Yuji ; Oshima, Hiroko ; Oshima, Masanobu ; Lee, Hyuk-Joon ; Kim, V Narry ; Chang, Aaron N ; Goel, Ajay ; Yang, Han-Kwang</creator><creatorcontrib>Han, Tae-Su ; Hur, Keun ; Xu, Guorong ; Choi, Boram ; Okugawa, Yoshinaga ; Toiyama, Yuji ; Oshima, Hiroko ; Oshima, Masanobu ; Lee, Hyuk-Joon ; Kim, V Narry ; Chang, Aaron N ; Goel, Ajay ; Yang, Han-Kwang</creatorcontrib><description>Objective Gastric cancer (GC) remains difficult to cure due to heterogeneity in a clinical challenge and the molecular mechanisms underlying this disease are complex and not completely understood. Accumulating evidence suggests that microRNAs (miRNAs) play an important role in GC, but the role of specific miRNAs involved in this disease remains elusive. We performed next generation sequencing (NGS)-based whole-transcriptome profiling to discover GC-specific miRNAs, followed by functional validation of results. Design NGS-based miRNA profiles were generated in matched pairs of GCs and adjacent normal mucosa (NM). Quantitative RT-PCR validation of miR-29c expression was performed in 274 gastric tissues, which included two cohorts of matched GC and NM specimens. Functional validation of miR-29c and its gene targets was undertaken in cell lines, as well as K19-C2mE and K19-Wnt1/C2mE transgenic mice. Results NGS analysis revealed four GC-specific miRNAs. Among these, miR-29c expression was significantly decreased in GC versus NM tissues (p<0.001). Ectopic expression of miR-29c mimics in GC cell lines resulted in reduced proliferation, adhesion, invasion and migration. High miR-29c expression suppressed xenograft tumour growth in nude mice. Direct interaction between miR-29c and its newly discovered target, ITGB1, was identified in cell lines and transgenic mice. MiR-29c expression demonstrated a stepwise decrease in wild type hyperplasia-dysplasia cascade in transgenic mice models of GC. Conclusions MiR-29c acts as a tumour suppressor in GC by directly targeting ITGB1. Loss of miR-29c expression is an early event in the initiation of gastric carcinogenesis and may serve as a diagnostic and therapeutic biomarker for patients with GC.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>DOI: 10.1136/gutjnl-2013-306640</identifier><identifier>PMID: 24870620</identifier><identifier>CODEN: GUTTAK</identifier><language>eng</language><publisher>England: BMJ Publishing Group LTD</publisher><subject>Animals ; Carcinogenesis - genetics ; Carcinogenesis - pathology ; Cell Adhesion - genetics ; Cell Movement - genetics ; Cell Proliferation - genetics ; Epigenetics ; Female ; Gastric cancer ; Gene expression ; Gene Expression Profiling - methods ; Gene Expression Regulation, Neoplastic ; Heterografts ; Hospitals ; Humans ; Integrin beta1 - genetics ; Medical diagnosis ; Medical prognosis ; Metastasis ; Mice, Nude ; Mice, Transgenic ; MicroRNAs ; MicroRNAs - genetics ; Neoplasm Invasiveness ; Neoplasm Transplantation ; Pathogenesis ; Patients ; RNA, Neoplasm - genetics ; Rodents ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology ; Studies ; Transcriptome ; Transgenic animals ; Tumor Cells, Cultured</subject><ispartof>Gut, 2015-02, Vol.64 (2), p.203-214</ispartof><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</rights><rights>Copyright: 2015 Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b637t-1a021f9d52754edd7ea1d1b280977ba33c4f8f450d4146acb087ef444c1989063</citedby><cites>FETCH-LOGICAL-b637t-1a021f9d52754edd7ea1d1b280977ba33c4f8f450d4146acb087ef444c1989063</cites><orcidid>0000-0002-6944-2718</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://gut.bmj.com/content/64/2/203.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://gut.bmj.com/content/64/2/203.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,230,314,723,776,780,881,3182,23551,27903,27904,53769,53771,77346,77377</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24870620$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Han, Tae-Su</creatorcontrib><creatorcontrib>Hur, Keun</creatorcontrib><creatorcontrib>Xu, Guorong</creatorcontrib><creatorcontrib>Choi, Boram</creatorcontrib><creatorcontrib>Okugawa, Yoshinaga</creatorcontrib><creatorcontrib>Toiyama, Yuji</creatorcontrib><creatorcontrib>Oshima, Hiroko</creatorcontrib><creatorcontrib>Oshima, Masanobu</creatorcontrib><creatorcontrib>Lee, Hyuk-Joon</creatorcontrib><creatorcontrib>Kim, V Narry</creatorcontrib><creatorcontrib>Chang, Aaron N</creatorcontrib><creatorcontrib>Goel, Ajay</creatorcontrib><creatorcontrib>Yang, Han-Kwang</creatorcontrib><title>MicroRNA-29c mediates initiation of gastric carcinogenesis by directly targeting ITGB1</title><title>Gut</title><addtitle>Gut</addtitle><description>Objective Gastric cancer (GC) remains difficult to cure due to heterogeneity in a clinical challenge and the molecular mechanisms underlying this disease are complex and not completely understood. Accumulating evidence suggests that microRNAs (miRNAs) play an important role in GC, but the role of specific miRNAs involved in this disease remains elusive. We performed next generation sequencing (NGS)-based whole-transcriptome profiling to discover GC-specific miRNAs, followed by functional validation of results. Design NGS-based miRNA profiles were generated in matched pairs of GCs and adjacent normal mucosa (NM). Quantitative RT-PCR validation of miR-29c expression was performed in 274 gastric tissues, which included two cohorts of matched GC and NM specimens. Functional validation of miR-29c and its gene targets was undertaken in cell lines, as well as K19-C2mE and K19-Wnt1/C2mE transgenic mice. Results NGS analysis revealed four GC-specific miRNAs. Among these, miR-29c expression was significantly decreased in GC versus NM tissues (p<0.001). Ectopic expression of miR-29c mimics in GC cell lines resulted in reduced proliferation, adhesion, invasion and migration. High miR-29c expression suppressed xenograft tumour growth in nude mice. Direct interaction between miR-29c and its newly discovered target, ITGB1, was identified in cell lines and transgenic mice. MiR-29c expression demonstrated a stepwise decrease in wild type hyperplasia-dysplasia cascade in transgenic mice models of GC. Conclusions MiR-29c acts as a tumour suppressor in GC by directly targeting ITGB1. Loss of miR-29c expression is an early event in the initiation of gastric carcinogenesis and may serve as a diagnostic and therapeutic biomarker for patients with GC.</description><subject>Animals</subject><subject>Carcinogenesis - genetics</subject><subject>Carcinogenesis - pathology</subject><subject>Cell Adhesion - genetics</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Epigenetics</subject><subject>Female</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Heterografts</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Integrin beta1 - genetics</subject><subject>Medical diagnosis</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Mice, Nude</subject><subject>Mice, Transgenic</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Transplantation</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>RNA, Neoplasm - genetics</subject><subject>Rodents</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><subject>Studies</subject><subject>Transcriptome</subject><subject>Transgenic animals</subject><subject>Tumor Cells, Cultured</subject><issn>0017-5749</issn><issn>1468-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkU1rFTEUhoMo9lr9Ay4k4MZNbL4mHxuhLVoLtQWpbkMmkxlzmZvUJCPcf28uU4t25SqBPOflvHkAeE3we0KYOJmWuo0zopgwxLAQHD8BG8KFQowq9RRsMCYSdZLrI_CilC3GWClNnoMjypXEguIN-P4luJy-Xp8iqh3c-SHY6gsMMdR2CynCNMLJlpqDg85mF2KafPQlFNjv4RCyd3Xew2rz5GuIE7y8vTgjL8Gz0c7Fv7o_j8G3Tx9vzz-jq5uLy_PTK9QLJisiFlMy6qGjsuN-GKS3ZCA9VVhL2VvGHB_VyDs88NbLuh4r6UfOuSNaaSzYMfiw5t4tfVve-Viznc1dDjub9ybZYP59ieGHmdIvw5ninOgW8O4-IKefiy_V7EJxfp5t9GkphiishJJSH9C3j9BtWnJs9QxpABddRw8UXan2raVkPz4sQ7A5aDOrNnPQZlZtbejN3zUeRv54agBagX63_Z_A3wOhoxQ</recordid><startdate>20150201</startdate><enddate>20150201</enddate><creator>Han, Tae-Su</creator><creator>Hur, 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LTD</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7T5</scope><scope>H94</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6944-2718</orcidid></search><sort><creationdate>20150201</creationdate><title>MicroRNA-29c mediates initiation of gastric carcinogenesis by directly targeting ITGB1</title><author>Han, Tae-Su ; Hur, Keun ; Xu, Guorong ; Choi, Boram ; Okugawa, Yoshinaga ; Toiyama, Yuji ; Oshima, Hiroko ; Oshima, Masanobu ; Lee, Hyuk-Joon ; Kim, V Narry ; Chang, Aaron N ; Goel, Ajay ; Yang, Han-Kwang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b637t-1a021f9d52754edd7ea1d1b280977ba33c4f8f450d4146acb087ef444c1989063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Carcinogenesis - genetics</topic><topic>Carcinogenesis - pathology</topic><topic>Cell Adhesion - genetics</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Epigenetics</topic><topic>Female</topic><topic>Gastric cancer</topic><topic>Gene expression</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Heterografts</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Integrin beta1 - genetics</topic><topic>Medical diagnosis</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Mice, Nude</topic><topic>Mice, Transgenic</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplasm Transplantation</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>RNA, Neoplasm - genetics</topic><topic>Rodents</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - pathology</topic><topic>Studies</topic><topic>Transcriptome</topic><topic>Transgenic animals</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Han, Tae-Su</creatorcontrib><creatorcontrib>Hur, Keun</creatorcontrib><creatorcontrib>Xu, Guorong</creatorcontrib><creatorcontrib>Choi, Boram</creatorcontrib><creatorcontrib>Okugawa, Yoshinaga</creatorcontrib><creatorcontrib>Toiyama, Yuji</creatorcontrib><creatorcontrib>Oshima, Hiroko</creatorcontrib><creatorcontrib>Oshima, Masanobu</creatorcontrib><creatorcontrib>Lee, Hyuk-Joon</creatorcontrib><creatorcontrib>Kim, V Narry</creatorcontrib><creatorcontrib>Chang, Aaron N</creatorcontrib><creatorcontrib>Goel, Ajay</creatorcontrib><creatorcontrib>Yang, Han-Kwang</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech 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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database (ProQuest)</collection><collection>Biological Science 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>ProQuest Central Basic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Han, Tae-Su</au><au>Hur, Keun</au><au>Xu, Guorong</au><au>Choi, Boram</au><au>Okugawa, Yoshinaga</au><au>Toiyama, Yuji</au><au>Oshima, Hiroko</au><au>Oshima, Masanobu</au><au>Lee, Hyuk-Joon</au><au>Kim, V Narry</au><au>Chang, Aaron N</au><au>Goel, Ajay</au><au>Yang, Han-Kwang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-29c mediates initiation of gastric carcinogenesis by directly targeting ITGB1</atitle><jtitle>Gut</jtitle><addtitle>Gut</addtitle><date>2015-02-01</date><risdate>2015</risdate><volume>64</volume><issue>2</issue><spage>203</spage><epage>214</epage><pages>203-214</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><coden>GUTTAK</coden><abstract>Objective Gastric cancer (GC) remains difficult to cure due to heterogeneity in a clinical challenge and the molecular mechanisms underlying this disease are complex and not completely understood. Accumulating evidence suggests that microRNAs (miRNAs) play an important role in GC, but the role of specific miRNAs involved in this disease remains elusive. We performed next generation sequencing (NGS)-based whole-transcriptome profiling to discover GC-specific miRNAs, followed by functional validation of results. Design NGS-based miRNA profiles were generated in matched pairs of GCs and adjacent normal mucosa (NM). Quantitative RT-PCR validation of miR-29c expression was performed in 274 gastric tissues, which included two cohorts of matched GC and NM specimens. Functional validation of miR-29c and its gene targets was undertaken in cell lines, as well as K19-C2mE and K19-Wnt1/C2mE transgenic mice. Results NGS analysis revealed four GC-specific miRNAs. Among these, miR-29c expression was significantly decreased in GC versus NM tissues (p<0.001). Ectopic expression of miR-29c mimics in GC cell lines resulted in reduced proliferation, adhesion, invasion and migration. High miR-29c expression suppressed xenograft tumour growth in nude mice. Direct interaction between miR-29c and its newly discovered target, ITGB1, was identified in cell lines and transgenic mice. MiR-29c expression demonstrated a stepwise decrease in wild type hyperplasia-dysplasia cascade in transgenic mice models of GC. Conclusions MiR-29c acts as a tumour suppressor in GC by directly targeting ITGB1. Loss of miR-29c expression is an early event in the initiation of gastric carcinogenesis and may serve as a diagnostic and therapeutic biomarker for patients with GC.</abstract><cop>England</cop><pub>BMJ Publishing Group LTD</pub><pmid>24870620</pmid><doi>10.1136/gutjnl-2013-306640</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-6944-2718</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Carcinogenesis - genetics Carcinogenesis - pathology Cell Adhesion - genetics Cell Movement - genetics Cell Proliferation - genetics Epigenetics Female Gastric cancer Gene expression Gene Expression Profiling - methods Gene Expression Regulation, Neoplastic Heterografts Hospitals Humans Integrin beta1 - genetics Medical diagnosis Medical prognosis Metastasis Mice, Nude Mice, Transgenic MicroRNAs MicroRNAs - genetics Neoplasm Invasiveness Neoplasm Transplantation Pathogenesis Patients RNA, Neoplasm - genetics Rodents Stomach Neoplasms - genetics Stomach Neoplasms - pathology Studies Transcriptome Transgenic animals Tumor Cells, Cultured |
| title | MicroRNA-29c mediates initiation of gastric carcinogenesis by directly targeting ITGB1 |
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