VEZT, a novel putative tumor suppressor, suppresses the growth and tumorigenicity of gastric cancer
Vezatin (VEZT), an adherens junctions transmembrane protein, was identified as a putative tumor suppressor in our previous study. However, the role of VEZT in tumorigenesis remains elusive. We aimed to clarify its epigenetic regulation and biological functions in gastric cancer. In this study, we sh...
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| description | Vezatin (VEZT), an adherens junctions transmembrane protein, was identified as a putative tumor suppressor in our previous study. However, the role of VEZT in tumorigenesis remains elusive. We aimed to clarify its epigenetic regulation and biological functions in gastric cancer. In this study, we show that the expression level of VEZT is involved in lymphatic metastasis, depth of cancer invasion and TNM stage in 104 gastric cancer patients. Bisulfate sequencing polymerase chain reaction (BSP) methods showed that VEZT was hypermethylated in tissues and corresponding blood of gastric cancer patients compared with healthy controls. Helicobacter pylori (H. pylori) infection induces the methylation and silencing of VEZT in GES-1 cells. Restoring VEZT expression in MKN-45 and NCI-N87 gastric cancer cells inhibited growth, invasion and tumorigenesis in vitro and in vivo. Global microarray analysis was applied to analyze the molecular basis of the biological functions of VEZT after VEZT transfection combined with real-time PCR and chromatin immunoprecipitation assay. G protein-coupled receptor 56(GPR56), cell growth, cell division cycle 42(CDC42), migration/invasion and transcription factor 19(TCF19), cell cycle progression, were identified as direct VEZT target genes. TCF19, a novel target of VEZT, was functionally validated. Overexpression of TCF19 in MKN-45 cells increased cell cycle progress and growth ability. This study provides novel insight into the regulation of the VEZT gene, which could represent a potential target for therapeutic anti-cancer strategies. |
| doi_str_mv | 10.1371/journal.pone.0074409 |
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However, the role of VEZT in tumorigenesis remains elusive. We aimed to clarify its epigenetic regulation and biological functions in gastric cancer. In this study, we show that the expression level of VEZT is involved in lymphatic metastasis, depth of cancer invasion and TNM stage in 104 gastric cancer patients. Bisulfate sequencing polymerase chain reaction (BSP) methods showed that VEZT was hypermethylated in tissues and corresponding blood of gastric cancer patients compared with healthy controls. Helicobacter pylori (H. pylori) infection induces the methylation and silencing of VEZT in GES-1 cells. Restoring VEZT expression in MKN-45 and NCI-N87 gastric cancer cells inhibited growth, invasion and tumorigenesis in vitro and in vivo. Global microarray analysis was applied to analyze the molecular basis of the biological functions of VEZT after VEZT transfection combined with real-time PCR and chromatin immunoprecipitation assay. G protein-coupled receptor 56(GPR56), cell growth, cell division cycle 42(CDC42), migration/invasion and transcription factor 19(TCF19), cell cycle progression, were identified as direct VEZT target genes. TCF19, a novel target of VEZT, was functionally validated. Overexpression of TCF19 in MKN-45 cells increased cell cycle progress and growth ability. This study provides novel insight into the regulation of the VEZT gene, which could represent a potential target for therapeutic anti-cancer strategies.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0074409</identifier><identifier>PMID: 24069310</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adherens junctions ; Aged ; Aged, 80 and over ; Analysis ; Animals ; Cancer ; Carrier Proteins - genetics ; Carrier Proteins - metabolism ; Case-Control Studies ; Cdc42 protein ; Cell adhesion & migration ; Cell cycle ; Cell division ; Cell Line, Tumor ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Chromatin ; Cluster Analysis ; Disease Models, Animal ; DNA Methylation ; DNA microarrays ; Epigenetic inheritance ; Epigenetics ; Female ; Gastric cancer ; Gastrointestinal surgery ; Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Genes ; Growth ; Health aspects ; Helicobacter Infections - genetics ; Helicobacter pylori ; Humans ; Immunoprecipitation ; Infection ; Infections ; Lasers ; Lymphatic Metastasis ; Male ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Metastases ; Methylation ; Mice ; Middle Aged ; Patients ; Polymerase chain reaction ; Reproducibility of Results ; Stomach cancer ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology ; Target recognition ; Tissues ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Transfection ; Tumor Burden ; Tumor suppressor genes ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism ; Tumorigenesis ; Tumorigenicity ; Tumors ; Xenograft Model Antitumor Assays</subject><ispartof>PloS one, 2013-09, Vol.8 (9), p.e74409</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Miao et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://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>2013 Miao et al 2013 Miao et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-7f61af2f21e59d11b47b4312cd79f35e651dbd9f555d737e1d0e8462452a47233</citedby><cites>FETCH-LOGICAL-c692t-7f61af2f21e59d11b47b4312cd79f35e651dbd9f555d737e1d0e8462452a47233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3775783/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3775783/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2926,23865,27923,27924,53790,53792,79371,79372</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24069310$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Katoh, Masaru</contributor><creatorcontrib>Miao, Ruizhen</creatorcontrib><creatorcontrib>Guo, Xiaobo</creatorcontrib><creatorcontrib>Zhi, Qiaoming</creatorcontrib><creatorcontrib>Shi, Yulong</creatorcontrib><creatorcontrib>Li, Leping</creatorcontrib><creatorcontrib>Mao, Xuehui</creatorcontrib><creatorcontrib>Zhang, Li</creatorcontrib><creatorcontrib>Li, Chensheng</creatorcontrib><title>VEZT, a novel putative tumor suppressor, suppresses the growth and tumorigenicity of gastric cancer</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Vezatin (VEZT), an adherens junctions transmembrane protein, was identified as a putative tumor suppressor in our previous study. However, the role of VEZT in tumorigenesis remains elusive. We aimed to clarify its epigenetic regulation and biological functions in gastric cancer. In this study, we show that the expression level of VEZT is involved in lymphatic metastasis, depth of cancer invasion and TNM stage in 104 gastric cancer patients. Bisulfate sequencing polymerase chain reaction (BSP) methods showed that VEZT was hypermethylated in tissues and corresponding blood of gastric cancer patients compared with healthy controls. Helicobacter pylori (H. pylori) infection induces the methylation and silencing of VEZT in GES-1 cells. Restoring VEZT expression in MKN-45 and NCI-N87 gastric cancer cells inhibited growth, invasion and tumorigenesis in vitro and in vivo. Global microarray analysis was applied to analyze the molecular basis of the biological functions of VEZT after VEZT transfection combined with real-time PCR and chromatin immunoprecipitation assay. G protein-coupled receptor 56(GPR56), cell growth, cell division cycle 42(CDC42), migration/invasion and transcription factor 19(TCF19), cell cycle progression, were identified as direct VEZT target genes. TCF19, a novel target of VEZT, was functionally validated. Overexpression of TCF19 in MKN-45 cells increased cell cycle progress and growth ability. This study provides novel insight into the regulation of the VEZT gene, which could represent a potential target for therapeutic anti-cancer strategies.</description><subject>Adherens junctions</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Analysis</subject><subject>Animals</subject><subject>Cancer</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - metabolism</subject><subject>Case-Control Studies</subject><subject>Cdc42 protein</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell division</subject><subject>Cell Line, Tumor</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Chromatin</subject><subject>Cluster Analysis</subject><subject>Disease Models, Animal</subject><subject>DNA Methylation</subject><subject>DNA microarrays</subject><subject>Epigenetic inheritance</subject><subject>Epigenetics</subject><subject>Female</subject><subject>Gastric cancer</subject><subject>Gastrointestinal surgery</subject><subject>Gene Expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Silencing</subject><subject>Genes</subject><subject>Growth</subject><subject>Health aspects</subject><subject>Helicobacter Infections - genetics</subject><subject>Helicobacter pylori</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Infection</subject><subject>Infections</subject><subject>Lasers</subject><subject>Lymphatic Metastasis</subject><subject>Male</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Metastases</subject><subject>Methylation</subject><subject>Mice</subject><subject>Middle Aged</subject><subject>Patients</subject><subject>Polymerase chain reaction</subject><subject>Reproducibility of Results</subject><subject>Stomach cancer</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><subject>Target recognition</subject><subject>Tissues</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Transfection</subject><subject>Tumor Burden</subject><subject>Tumor suppressor genes</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>Tumorigenesis</subject><subject>Tumorigenicity</subject><subject>Tumors</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</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><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7rr6D0QDgiDsjPlq094Iy7LqwMKCrnvhTUjz0WboNDVJR_ffm3G6wxQUJBc5nDznTfLyZtlLBJeIMPR-7Ubfi245uF4vIWSUwupRdooqghcFhuTxUX2SPQthDWFOyqJ4mp1gCouKIHiaybur77fnQIDebXUHhjGKaLcaxHHjPAjjMHgdgvPnh1oHEFsNGu9-xhaIXu1Z2-jeShvvgTOgESF6K4EUvdT-efbEiC7oF9N-ln37eHV7-XlxffNpdXlxvZBFheOCmQIJgw1GOq8UQjVlNSUIS8UqQ3Jd5EjVqjJ5nitGmEYK6pIWmOZYUIYJOcte73WHzgU--RM4ooSWRYlpmYjVnlBOrPng7Ub4e-6E5X8azjdc-GhlpzlDOaHK1HWhEDWQJbtIjZgQUtU61Unrw3TbWG-0krqPXnQz0flJb1veuC0njOWs3Am8mQS8-zHqEP_x5IlqRHqV7Y1LYnJjg-QXlJXp25ChRC3_QqWl9MbKlBBjU3828G42kJiof8VGjCHw1dcv_8_e3M3Zt0dsq0UX2-C6MVrXhzlI96D0LgSvzcE5BPku4A9u8F3A-RTwNPbq2PXD0EOiyW-SafYy</recordid><startdate>20130917</startdate><enddate>20130917</enddate><creator>Miao, Ruizhen</creator><creator>Guo, Xiaobo</creator><creator>Zhi, Qiaoming</creator><creator>Shi, Yulong</creator><creator>Li, Leping</creator><creator>Mao, Xuehui</creator><creator>Zhang, Li</creator><creator>Li, Chensheng</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>IOV</scope><scope>ISR</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>AEUYN</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>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130917</creationdate><title>VEZT, a novel putative tumor suppressor, suppresses the growth and tumorigenicity of gastric cancer</title><author>Miao, Ruizhen ; Guo, Xiaobo ; Zhi, Qiaoming ; Shi, Yulong ; Li, Leping ; Mao, Xuehui ; Zhang, Li ; Li, Chensheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-7f61af2f21e59d11b47b4312cd79f35e651dbd9f555d737e1d0e8462452a47233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adherens junctions</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Analysis</topic><topic>Animals</topic><topic>Cancer</topic><topic>Carrier Proteins - genetics</topic><topic>Carrier Proteins - metabolism</topic><topic>Case-Control Studies</topic><topic>Cdc42 protein</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cell division</topic><topic>Cell Line, Tumor</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Chromatin</topic><topic>Cluster Analysis</topic><topic>Disease Models, Animal</topic><topic>DNA Methylation</topic><topic>DNA microarrays</topic><topic>Epigenetic inheritance</topic><topic>Epigenetics</topic><topic>Female</topic><topic>Gastric cancer</topic><topic>Gastrointestinal surgery</topic><topic>Gene Expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Silencing</topic><topic>Genes</topic><topic>Growth</topic><topic>Health aspects</topic><topic>Helicobacter Infections - genetics</topic><topic>Helicobacter pylori</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Infection</topic><topic>Infections</topic><topic>Lasers</topic><topic>Lymphatic Metastasis</topic><topic>Male</topic><topic>Membrane Proteins - 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However, the role of VEZT in tumorigenesis remains elusive. We aimed to clarify its epigenetic regulation and biological functions in gastric cancer. In this study, we show that the expression level of VEZT is involved in lymphatic metastasis, depth of cancer invasion and TNM stage in 104 gastric cancer patients. Bisulfate sequencing polymerase chain reaction (BSP) methods showed that VEZT was hypermethylated in tissues and corresponding blood of gastric cancer patients compared with healthy controls. Helicobacter pylori (H. pylori) infection induces the methylation and silencing of VEZT in GES-1 cells. Restoring VEZT expression in MKN-45 and NCI-N87 gastric cancer cells inhibited growth, invasion and tumorigenesis in vitro and in vivo. Global microarray analysis was applied to analyze the molecular basis of the biological functions of VEZT after VEZT transfection combined with real-time PCR and chromatin immunoprecipitation assay. G protein-coupled receptor 56(GPR56), cell growth, cell division cycle 42(CDC42), migration/invasion and transcription factor 19(TCF19), cell cycle progression, were identified as direct VEZT target genes. TCF19, a novel target of VEZT, was functionally validated. Overexpression of TCF19 in MKN-45 cells increased cell cycle progress and growth ability. This study provides novel insight into the regulation of the VEZT gene, which could represent a potential target for therapeutic anti-cancer strategies.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24069310</pmid><doi>10.1371/journal.pone.0074409</doi><tpages>e74409</tpages><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1434868248 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adherens junctions Aged Aged, 80 and over Analysis Animals Cancer Carrier Proteins - genetics Carrier Proteins - metabolism Case-Control Studies Cdc42 protein Cell adhesion & migration Cell cycle Cell division Cell Line, Tumor Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Chromatin Cluster Analysis Disease Models, Animal DNA Methylation DNA microarrays Epigenetic inheritance Epigenetics Female Gastric cancer Gastrointestinal surgery Gene Expression Gene Expression Profiling Gene Expression Regulation, Neoplastic Gene Silencing Genes Growth Health aspects Helicobacter Infections - genetics Helicobacter pylori Humans Immunoprecipitation Infection Infections Lasers Lymphatic Metastasis Male Membrane Proteins - genetics Membrane Proteins - metabolism Metastases Methylation Mice Middle Aged Patients Polymerase chain reaction Reproducibility of Results Stomach cancer Stomach Neoplasms - genetics Stomach Neoplasms - pathology Target recognition Tissues Transcription Factors - genetics Transcription Factors - metabolism Transfection Tumor Burden Tumor suppressor genes Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism Tumorigenesis Tumorigenicity Tumors Xenograft Model Antitumor Assays |
| title | VEZT, a novel putative tumor suppressor, suppresses the growth and tumorigenicity of gastric cancer |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-13T09%3A58%3A38IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=VEZT,%20a%20novel%20putative%20tumor%20suppressor,%20suppresses%20the%20growth%20and%20tumorigenicity%20of%20gastric%20cancer&rft.jtitle=PloS%20one&rft.au=Miao,%20Ruizhen&rft.date=2013-09-17&rft.volume=8&rft.issue=9&rft.spage=e74409&rft.pages=e74409-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0074409&rft_dat=%3Cgale_plos_%3EA478233071%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1434868248&rft_id=info:pmid/24069310&rft_galeid=A478233071&rft_doaj_id=oai_doaj_org_article_71534dfbb6d14f079313b17aacdbe313&rfr_iscdi=true |