Transmembrane Channel-Like 5 (TMC5) promotes prostate cancer cell proliferation through cell cycle regulation
In this study, we aimed to investigate the biological functions of Transmembrane Channel-Like 5 (TMC5) by bioinformatics and molecular biology methods in prostate cancer (PCa). We assessed the mRNA expression level of TMC5 in PCa with public database the Cancer Genome Atlas (TCGA) and Oncomine. The...
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| Veröffentlicht in: | Biochimie 2019-10, Vol.165, p.115-122 |
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| creator | Zhang, Wanfeng Wang, Sen Zhang, Xianqin Liu, Kun Song, Jing Leng, Xue Luo, Ruihan Ran, Longke |
| description | In this study, we aimed to investigate the biological functions of Transmembrane Channel-Like 5 (TMC5) by bioinformatics and molecular biology methods in prostate cancer (PCa).
We assessed the mRNA expression level of TMC5 in PCa with public database the Cancer Genome Atlas (TCGA) and Oncomine. The biological functions were demonstrated by bioinformatics methods and siRNA mediated knockdown experiments. Reverse transcription polymerase chain reaction (RT-PCR), immunohistochemical (IHC) experiments and microarray analysis were performed to confirm the results.
TMC5 expression level was significantly up-regulated in 4 independent PCa cohorts compared to normal group. Moreover, TMC5 has higher diagnostic efficiency than PSA-KLK3 (AUC (Area Under Curve) = 0.772, P |
| doi_str_mv | 10.1016/j.biochi.2019.07.017 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2267012692</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0300908419302172</els_id><sourcerecordid>2267012692</sourcerecordid><originalsourceid>FETCH-LOGICAL-c362t-4720eb34485b7e18cba3579f0966fdae149d37490e6eab2b5661a7a124e435eb3</originalsourceid><addsrcrecordid>eNp9kMtO5DAQRa0RaGiY-YMRypJZJJQfsZMNEmoND6kRm5615TgV2k0eYCdI_D0OAZasquS611X3EPKHQkaByvN9VrnB7lzGgJYZqAyo-kFWVPIilbTgB2QFHCAtoRBH5DiEPQDkwMqf5IhTnstCqBXptt70ocOuihWT9c70Pbbpxj1ikidn27t1_jd58kM3jBjmJoxmxMSa3qJPLLbt_Ni6Br0Z3dAn484P08NuGdlX22Li8WFq36e_yGFj2oC_P-oJ-X_1b7u-STf317fry01quWRjKhQDrLgQRV4ppIWtDM9V2UApZVMbpKKsuRIloERTsSqXkhplKBMoeB6dJ-Rs-Tfe9jxhGHXnwnxRzDhMQTMmFVAmSxalYpHamC14bPSTd53xr5qCnkHrvV5A6xm0BqUj6Gg7_dgwVR3WX6ZPslFwsQgw5nxx6HWwDiO12nm0o64H9_2GN5P3kT0</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2267012692</pqid></control><display><type>article</type><title>Transmembrane Channel-Like 5 (TMC5) promotes prostate cancer cell proliferation through cell cycle regulation</title><source>MEDLINE</source><source>ScienceDirect Journals (5 years ago - present)</source><creator>Zhang, Wanfeng ; Wang, Sen ; Zhang, Xianqin ; Liu, Kun ; Song, Jing ; Leng, Xue ; Luo, Ruihan ; Ran, Longke</creator><creatorcontrib>Zhang, Wanfeng ; Wang, Sen ; Zhang, Xianqin ; Liu, Kun ; Song, Jing ; Leng, Xue ; Luo, Ruihan ; Ran, Longke</creatorcontrib><description>In this study, we aimed to investigate the biological functions of Transmembrane Channel-Like 5 (TMC5) by bioinformatics and molecular biology methods in prostate cancer (PCa).
We assessed the mRNA expression level of TMC5 in PCa with public database the Cancer Genome Atlas (TCGA) and Oncomine. The biological functions were demonstrated by bioinformatics methods and siRNA mediated knockdown experiments. Reverse transcription polymerase chain reaction (RT-PCR), immunohistochemical (IHC) experiments and microarray analysis were performed to confirm the results.
TMC5 expression level was significantly up-regulated in 4 independent PCa cohorts compared to normal group. Moreover, TMC5 has higher diagnostic efficiency than PSA-KLK3 (AUC (Area Under Curve) = 0.772, P < 0.001). The high expression of TMC5 was associated with clinical Gleason score, prostate-specific antigen (PSA) level, androgen receptor (AR) activity score and the genes which were known frequently mutated in PCa progression (P < 0.05). Functionally, Gene Otology (GO) analysis suggested that TMC5 was related to cell development; TMC5 knockdown significantly inhibited PCa cells proliferation by arresting cell cycle at G1 phase. Drug sensitivity experiments showed TMC5 knockdown significantly enhanced cells sensitivity to 5-Fluorouracil. Microarray analysis showed TMC5 knockdown significantly inhibited cell cycle and tumor progression.
Our findings revealed that TMC5 promoted PCa cell proliferation through cell cycle regulation and could be a powerful and hopeful target for PCa treatment.
•TMC5 is upregulated in PCa.•TMC5 promoted PCa cells proliferation by regulating cell cycle.•Knockdown of TMC5 enhanced drug sensitivity to 5-Fluorouracil in PCa.</description><identifier>ISSN: 0300-9084</identifier><identifier>EISSN: 1638-6183</identifier><identifier>DOI: 10.1016/j.biochi.2019.07.017</identifier><identifier>PMID: 31356847</identifier><language>eng</language><publisher>France: Elsevier B.V</publisher><subject>Cell cycle ; Cell Cycle Checkpoints ; Cell Line, Tumor ; Cell Proliferation ; Diagnosis ; Gene Expression Regulation, Neoplastic ; Humans ; Ion Channels - genetics ; Ion Channels - physiology ; Male ; Proliferation ; Prostate cancer ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Signal Transduction ; TMC5</subject><ispartof>Biochimie, 2019-10, Vol.165, p.115-122</ispartof><rights>2019</rights><rights>Copyright © 2019. Published by Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-4720eb34485b7e18cba3579f0966fdae149d37490e6eab2b5661a7a124e435eb3</citedby><cites>FETCH-LOGICAL-c362t-4720eb34485b7e18cba3579f0966fdae149d37490e6eab2b5661a7a124e435eb3</cites><orcidid>0000-0002-7290-8478 ; 0000-0002-8717-1552 ; 0000-0001-5997-4051 ; 0000-0002-8704-1758 ; 0000-0002-6434-5521 ; 0000-0003-1475-5263 ; 0000-0001-6358-1672 ; 0000-0001-6173-5981</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.biochi.2019.07.017$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31356847$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Wanfeng</creatorcontrib><creatorcontrib>Wang, Sen</creatorcontrib><creatorcontrib>Zhang, Xianqin</creatorcontrib><creatorcontrib>Liu, Kun</creatorcontrib><creatorcontrib>Song, Jing</creatorcontrib><creatorcontrib>Leng, Xue</creatorcontrib><creatorcontrib>Luo, Ruihan</creatorcontrib><creatorcontrib>Ran, Longke</creatorcontrib><title>Transmembrane Channel-Like 5 (TMC5) promotes prostate cancer cell proliferation through cell cycle regulation</title><title>Biochimie</title><addtitle>Biochimie</addtitle><description>In this study, we aimed to investigate the biological functions of Transmembrane Channel-Like 5 (TMC5) by bioinformatics and molecular biology methods in prostate cancer (PCa).
We assessed the mRNA expression level of TMC5 in PCa with public database the Cancer Genome Atlas (TCGA) and Oncomine. The biological functions were demonstrated by bioinformatics methods and siRNA mediated knockdown experiments. Reverse transcription polymerase chain reaction (RT-PCR), immunohistochemical (IHC) experiments and microarray analysis were performed to confirm the results.
TMC5 expression level was significantly up-regulated in 4 independent PCa cohorts compared to normal group. Moreover, TMC5 has higher diagnostic efficiency than PSA-KLK3 (AUC (Area Under Curve) = 0.772, P < 0.001). The high expression of TMC5 was associated with clinical Gleason score, prostate-specific antigen (PSA) level, androgen receptor (AR) activity score and the genes which were known frequently mutated in PCa progression (P < 0.05). Functionally, Gene Otology (GO) analysis suggested that TMC5 was related to cell development; TMC5 knockdown significantly inhibited PCa cells proliferation by arresting cell cycle at G1 phase. Drug sensitivity experiments showed TMC5 knockdown significantly enhanced cells sensitivity to 5-Fluorouracil. Microarray analysis showed TMC5 knockdown significantly inhibited cell cycle and tumor progression.
Our findings revealed that TMC5 promoted PCa cell proliferation through cell cycle regulation and could be a powerful and hopeful target for PCa treatment.
•TMC5 is upregulated in PCa.•TMC5 promoted PCa cells proliferation by regulating cell cycle.•Knockdown of TMC5 enhanced drug sensitivity to 5-Fluorouracil in PCa.</description><subject>Cell cycle</subject><subject>Cell Cycle Checkpoints</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Diagnosis</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Ion Channels - genetics</subject><subject>Ion Channels - physiology</subject><subject>Male</subject><subject>Proliferation</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Signal Transduction</subject><subject>TMC5</subject><issn>0300-9084</issn><issn>1638-6183</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtO5DAQRa0RaGiY-YMRypJZJJQfsZMNEmoND6kRm5615TgV2k0eYCdI_D0OAZasquS611X3EPKHQkaByvN9VrnB7lzGgJYZqAyo-kFWVPIilbTgB2QFHCAtoRBH5DiEPQDkwMqf5IhTnstCqBXptt70ocOuihWT9c70Pbbpxj1ikidn27t1_jd58kM3jBjmJoxmxMSa3qJPLLbt_Ni6Br0Z3dAn484P08NuGdlX22Li8WFq36e_yGFj2oC_P-oJ-X_1b7u-STf317fry01quWRjKhQDrLgQRV4ppIWtDM9V2UApZVMbpKKsuRIloERTsSqXkhplKBMoeB6dJ-Rs-Tfe9jxhGHXnwnxRzDhMQTMmFVAmSxalYpHamC14bPSTd53xr5qCnkHrvV5A6xm0BqUj6Gg7_dgwVR3WX6ZPslFwsQgw5nxx6HWwDiO12nm0o64H9_2GN5P3kT0</recordid><startdate>201910</startdate><enddate>201910</enddate><creator>Zhang, Wanfeng</creator><creator>Wang, Sen</creator><creator>Zhang, Xianqin</creator><creator>Liu, Kun</creator><creator>Song, Jing</creator><creator>Leng, Xue</creator><creator>Luo, Ruihan</creator><creator>Ran, Longke</creator><general>Elsevier B.V</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>7X8</scope><orcidid>https://orcid.org/0000-0002-7290-8478</orcidid><orcidid>https://orcid.org/0000-0002-8717-1552</orcidid><orcidid>https://orcid.org/0000-0001-5997-4051</orcidid><orcidid>https://orcid.org/0000-0002-8704-1758</orcidid><orcidid>https://orcid.org/0000-0002-6434-5521</orcidid><orcidid>https://orcid.org/0000-0003-1475-5263</orcidid><orcidid>https://orcid.org/0000-0001-6358-1672</orcidid><orcidid>https://orcid.org/0000-0001-6173-5981</orcidid></search><sort><creationdate>201910</creationdate><title>Transmembrane Channel-Like 5 (TMC5) promotes prostate cancer cell proliferation through cell cycle regulation</title><author>Zhang, Wanfeng ; Wang, Sen ; Zhang, Xianqin ; Liu, Kun ; Song, Jing ; Leng, Xue ; Luo, Ruihan ; Ran, Longke</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-4720eb34485b7e18cba3579f0966fdae149d37490e6eab2b5661a7a124e435eb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Cell cycle</topic><topic>Cell Cycle Checkpoints</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Diagnosis</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Ion Channels - genetics</topic><topic>Ion Channels - physiology</topic><topic>Male</topic><topic>Proliferation</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Signal Transduction</topic><topic>TMC5</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Wanfeng</creatorcontrib><creatorcontrib>Wang, Sen</creatorcontrib><creatorcontrib>Zhang, Xianqin</creatorcontrib><creatorcontrib>Liu, Kun</creatorcontrib><creatorcontrib>Song, Jing</creatorcontrib><creatorcontrib>Leng, Xue</creatorcontrib><creatorcontrib>Luo, Ruihan</creatorcontrib><creatorcontrib>Ran, Longke</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochimie</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Wanfeng</au><au>Wang, Sen</au><au>Zhang, Xianqin</au><au>Liu, Kun</au><au>Song, Jing</au><au>Leng, Xue</au><au>Luo, Ruihan</au><au>Ran, Longke</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transmembrane Channel-Like 5 (TMC5) promotes prostate cancer cell proliferation through cell cycle regulation</atitle><jtitle>Biochimie</jtitle><addtitle>Biochimie</addtitle><date>2019-10</date><risdate>2019</risdate><volume>165</volume><spage>115</spage><epage>122</epage><pages>115-122</pages><issn>0300-9084</issn><eissn>1638-6183</eissn><abstract>In this study, we aimed to investigate the biological functions of Transmembrane Channel-Like 5 (TMC5) by bioinformatics and molecular biology methods in prostate cancer (PCa).
We assessed the mRNA expression level of TMC5 in PCa with public database the Cancer Genome Atlas (TCGA) and Oncomine. The biological functions were demonstrated by bioinformatics methods and siRNA mediated knockdown experiments. Reverse transcription polymerase chain reaction (RT-PCR), immunohistochemical (IHC) experiments and microarray analysis were performed to confirm the results.
TMC5 expression level was significantly up-regulated in 4 independent PCa cohorts compared to normal group. Moreover, TMC5 has higher diagnostic efficiency than PSA-KLK3 (AUC (Area Under Curve) = 0.772, P < 0.001). The high expression of TMC5 was associated with clinical Gleason score, prostate-specific antigen (PSA) level, androgen receptor (AR) activity score and the genes which were known frequently mutated in PCa progression (P < 0.05). Functionally, Gene Otology (GO) analysis suggested that TMC5 was related to cell development; TMC5 knockdown significantly inhibited PCa cells proliferation by arresting cell cycle at G1 phase. Drug sensitivity experiments showed TMC5 knockdown significantly enhanced cells sensitivity to 5-Fluorouracil. Microarray analysis showed TMC5 knockdown significantly inhibited cell cycle and tumor progression.
Our findings revealed that TMC5 promoted PCa cell proliferation through cell cycle regulation and could be a powerful and hopeful target for PCa treatment.
•TMC5 is upregulated in PCa.•TMC5 promoted PCa cells proliferation by regulating cell cycle.•Knockdown of TMC5 enhanced drug sensitivity to 5-Fluorouracil in PCa.</abstract><cop>France</cop><pub>Elsevier B.V</pub><pmid>31356847</pmid><doi>10.1016/j.biochi.2019.07.017</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-7290-8478</orcidid><orcidid>https://orcid.org/0000-0002-8717-1552</orcidid><orcidid>https://orcid.org/0000-0001-5997-4051</orcidid><orcidid>https://orcid.org/0000-0002-8704-1758</orcidid><orcidid>https://orcid.org/0000-0002-6434-5521</orcidid><orcidid>https://orcid.org/0000-0003-1475-5263</orcidid><orcidid>https://orcid.org/0000-0001-6358-1672</orcidid><orcidid>https://orcid.org/0000-0001-6173-5981</orcidid></addata></record> |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Cell cycle Cell Cycle Checkpoints Cell Line, Tumor Cell Proliferation Diagnosis Gene Expression Regulation, Neoplastic Humans Ion Channels - genetics Ion Channels - physiology Male Proliferation Prostate cancer Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Signal Transduction TMC5 |
| title | Transmembrane Channel-Like 5 (TMC5) promotes prostate cancer cell proliferation through cell cycle regulation |
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