High PRMT5 expression is associated with poor overall survival and tumor progression in bladder cancer
Arginine methyltransferase 5 (PRMT5) is involved in a variety of cancers. We used bioinformatics analysis to investigate PRMT5 overexpression in bladder urothelial cancer (BUC) and its clinical significance. We also conducted molecular biology experiments to investigate the effect of PRMT5 on the ph...
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Veröffentlicht in: | Aging (Albany, NY.) NY.), 2020-05, Vol.12 (9), p.8728-8741 |
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creator | Tan, Lei Xiao, Kanghua Ye, Yunlin Liang, Haitao Chen, Mingkun Luo, Junhang Qin, Zike |
description | Arginine methyltransferase 5 (PRMT5) is involved in a variety of cancers. We used bioinformatics analysis to investigate PRMT5 overexpression in bladder urothelial cancer (BUC) and its clinical significance. We also conducted molecular biology experiments to investigate the effect of PRMT5 on the phenotype of BUC cells in vitro and in vivo. PRMT5 was found to be upregulated in BUC tissue in the Oncomine and The Cancer Genome Atlas databases. We validated the results from these databases in a cohort of BUC samples. Kaplan-Meier and Cox multivariate analyses demonstrated that PRMT5 upregulation is an independent prognostic risk factor for BUC. The in vitro and in vivo phenotypic experiments found that downregulated expression of PRMT5 in BUC cells inhibits BUC cell proliferation and aggression. In addition, gene set enrichment analysis demonstrated that PRMT5 knockdown leads to cell cycle G1/S arrest, deactivation of Akt, and mTOR phosphorylation in BUC cells. These results suggest that PRMT5 could be used as a potential molecular marker for BUC in the future. |
doi_str_mv | 10.18632/aging.103198 |
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We used bioinformatics analysis to investigate PRMT5 overexpression in bladder urothelial cancer (BUC) and its clinical significance. We also conducted molecular biology experiments to investigate the effect of PRMT5 on the phenotype of BUC cells in vitro and in vivo. PRMT5 was found to be upregulated in BUC tissue in the Oncomine and The Cancer Genome Atlas databases. We validated the results from these databases in a cohort of BUC samples. Kaplan-Meier and Cox multivariate analyses demonstrated that PRMT5 upregulation is an independent prognostic risk factor for BUC. The in vitro and in vivo phenotypic experiments found that downregulated expression of PRMT5 in BUC cells inhibits BUC cell proliferation and aggression. In addition, gene set enrichment analysis demonstrated that PRMT5 knockdown leads to cell cycle G1/S arrest, deactivation of Akt, and mTOR phosphorylation in BUC cells. These results suggest that PRMT5 could be used as a potential molecular marker for BUC in the future.</description><identifier>ISSN: 1945-4589</identifier><identifier>EISSN: 1945-4589</identifier><identifier>DOI: 10.18632/aging.103198</identifier><identifier>PMID: 32392182</identifier><language>eng</language><publisher>United States: Impact Journals</publisher><subject>Animals ; Biomarkers, Tumor ; Cell Line, Tumor ; Cell Proliferation ; Databases, Factual ; Disease Progression ; Down-Regulation ; Female ; G1 Phase Cell Cycle Checkpoints ; Gene Expression ; Humans ; Male ; Mice, Inbred BALB C ; Mice, Nude ; Protein-Arginine N-Methyltransferases - genetics ; Protein-Arginine N-Methyltransferases - metabolism ; Research Paper ; Survival Analysis ; Up-Regulation ; Urinary Bladder Neoplasms - genetics ; Urinary Bladder Neoplasms - metabolism ; Urinary Bladder Neoplasms - mortality ; Urinary Bladder Neoplasms - pathology ; Xenograft Model Antitumor Assays</subject><ispartof>Aging (Albany, NY.), 2020-05, Vol.12 (9), p.8728-8741</ispartof><rights>Copyright © 2020 Tan et al.</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-4f1108850476a143d776eb3fd0c98e7c31ae4e30fc9046bce277c1db3af942563</citedby><cites>FETCH-LOGICAL-c387t-4f1108850476a143d776eb3fd0c98e7c31ae4e30fc9046bce277c1db3af942563</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/PMC7244052/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244052/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32392182$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tan, Lei</creatorcontrib><creatorcontrib>Xiao, Kanghua</creatorcontrib><creatorcontrib>Ye, Yunlin</creatorcontrib><creatorcontrib>Liang, Haitao</creatorcontrib><creatorcontrib>Chen, Mingkun</creatorcontrib><creatorcontrib>Luo, Junhang</creatorcontrib><creatorcontrib>Qin, Zike</creatorcontrib><title>High PRMT5 expression is associated with poor overall survival and tumor progression in bladder cancer</title><title>Aging (Albany, NY.)</title><addtitle>Aging (Albany NY)</addtitle><description>Arginine methyltransferase 5 (PRMT5) is involved in a variety of cancers. We used bioinformatics analysis to investigate PRMT5 overexpression in bladder urothelial cancer (BUC) and its clinical significance. We also conducted molecular biology experiments to investigate the effect of PRMT5 on the phenotype of BUC cells in vitro and in vivo. PRMT5 was found to be upregulated in BUC tissue in the Oncomine and The Cancer Genome Atlas databases. We validated the results from these databases in a cohort of BUC samples. Kaplan-Meier and Cox multivariate analyses demonstrated that PRMT5 upregulation is an independent prognostic risk factor for BUC. The in vitro and in vivo phenotypic experiments found that downregulated expression of PRMT5 in BUC cells inhibits BUC cell proliferation and aggression. In addition, gene set enrichment analysis demonstrated that PRMT5 knockdown leads to cell cycle G1/S arrest, deactivation of Akt, and mTOR phosphorylation in BUC cells. These results suggest that PRMT5 could be used as a potential molecular marker for BUC in the future.</description><subject>Animals</subject><subject>Biomarkers, Tumor</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Databases, Factual</subject><subject>Disease Progression</subject><subject>Down-Regulation</subject><subject>Female</subject><subject>G1 Phase Cell Cycle Checkpoints</subject><subject>Gene Expression</subject><subject>Humans</subject><subject>Male</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Protein-Arginine N-Methyltransferases - genetics</subject><subject>Protein-Arginine N-Methyltransferases - metabolism</subject><subject>Research Paper</subject><subject>Survival Analysis</subject><subject>Up-Regulation</subject><subject>Urinary Bladder Neoplasms - genetics</subject><subject>Urinary Bladder Neoplasms - metabolism</subject><subject>Urinary Bladder Neoplasms - mortality</subject><subject>Urinary Bladder Neoplasms - pathology</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1945-4589</issn><issn>1945-4589</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1LxDAQxYMofh-9So5eqvlqk14EEXWFFUX0HNJ02o10m5q0Vf97i6vLepqB95s3Dx5CJ5ScU5VxdmFq19bnlHCaqy20T3ORJiJV-fbGvocOYnwjJEtTke2iPc54zqhi-6iauXqBn54fXlIMn12AGJ1vsYvYxOitMz2U-MP1C9x5H7AfIZimwXEIoxtNg01b4n5YTlIXfL0-b3HRmLKEgK1pLYQjtFOZJsLx7zxEr7c3L9ezZP54d399NU8sV7JPREUpUSolQmaGCl5KmUHBq5LYXIG0nBoQwEllcyKywgKT0tKy4KbKBUszfoguV77dUCyhtND2U17dBbc04Ut74_R_pXULXftRSyYESdlkcPZrEPz7ALHXSxctNI1pwQ9RM0Go4pwoOqHJCrXBxxigWr-hRP90o3-60atuJv50M9ua_iuDfwOFW41U</recordid><startdate>20200511</startdate><enddate>20200511</enddate><creator>Tan, Lei</creator><creator>Xiao, Kanghua</creator><creator>Ye, Yunlin</creator><creator>Liang, Haitao</creator><creator>Chen, Mingkun</creator><creator>Luo, Junhang</creator><creator>Qin, Zike</creator><general>Impact Journals</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><scope>5PM</scope></search><sort><creationdate>20200511</creationdate><title>High PRMT5 expression is associated with poor overall survival and tumor progression in bladder cancer</title><author>Tan, Lei ; Xiao, Kanghua ; Ye, Yunlin ; Liang, Haitao ; Chen, Mingkun ; Luo, Junhang ; Qin, Zike</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-4f1108850476a143d776eb3fd0c98e7c31ae4e30fc9046bce277c1db3af942563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Biomarkers, Tumor</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Databases, Factual</topic><topic>Disease Progression</topic><topic>Down-Regulation</topic><topic>Female</topic><topic>G1 Phase Cell Cycle Checkpoints</topic><topic>Gene Expression</topic><topic>Humans</topic><topic>Male</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Protein-Arginine N-Methyltransferases - genetics</topic><topic>Protein-Arginine N-Methyltransferases - metabolism</topic><topic>Research Paper</topic><topic>Survival Analysis</topic><topic>Up-Regulation</topic><topic>Urinary Bladder Neoplasms - genetics</topic><topic>Urinary Bladder Neoplasms - metabolism</topic><topic>Urinary Bladder Neoplasms - mortality</topic><topic>Urinary Bladder Neoplasms - pathology</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>online_resources</toplevel><creatorcontrib>Tan, Lei</creatorcontrib><creatorcontrib>Xiao, Kanghua</creatorcontrib><creatorcontrib>Ye, Yunlin</creatorcontrib><creatorcontrib>Liang, Haitao</creatorcontrib><creatorcontrib>Chen, Mingkun</creatorcontrib><creatorcontrib>Luo, Junhang</creatorcontrib><creatorcontrib>Qin, Zike</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Aging (Albany, NY.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tan, Lei</au><au>Xiao, Kanghua</au><au>Ye, Yunlin</au><au>Liang, Haitao</au><au>Chen, Mingkun</au><au>Luo, Junhang</au><au>Qin, Zike</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High PRMT5 expression is associated with poor overall survival and tumor progression in bladder cancer</atitle><jtitle>Aging (Albany, NY.)</jtitle><addtitle>Aging (Albany NY)</addtitle><date>2020-05-11</date><risdate>2020</risdate><volume>12</volume><issue>9</issue><spage>8728</spage><epage>8741</epage><pages>8728-8741</pages><issn>1945-4589</issn><eissn>1945-4589</eissn><abstract>Arginine methyltransferase 5 (PRMT5) is involved in a variety of cancers. We used bioinformatics analysis to investigate PRMT5 overexpression in bladder urothelial cancer (BUC) and its clinical significance. We also conducted molecular biology experiments to investigate the effect of PRMT5 on the phenotype of BUC cells in vitro and in vivo. PRMT5 was found to be upregulated in BUC tissue in the Oncomine and The Cancer Genome Atlas databases. We validated the results from these databases in a cohort of BUC samples. Kaplan-Meier and Cox multivariate analyses demonstrated that PRMT5 upregulation is an independent prognostic risk factor for BUC. The in vitro and in vivo phenotypic experiments found that downregulated expression of PRMT5 in BUC cells inhibits BUC cell proliferation and aggression. In addition, gene set enrichment analysis demonstrated that PRMT5 knockdown leads to cell cycle G1/S arrest, deactivation of Akt, and mTOR phosphorylation in BUC cells. These results suggest that PRMT5 could be used as a potential molecular marker for BUC in the future.</abstract><cop>United States</cop><pub>Impact Journals</pub><pmid>32392182</pmid><doi>10.18632/aging.103198</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Biomarkers, Tumor Cell Line, Tumor Cell Proliferation Databases, Factual Disease Progression Down-Regulation Female G1 Phase Cell Cycle Checkpoints Gene Expression Humans Male Mice, Inbred BALB C Mice, Nude Protein-Arginine N-Methyltransferases - genetics Protein-Arginine N-Methyltransferases - metabolism Research Paper Survival Analysis Up-Regulation Urinary Bladder Neoplasms - genetics Urinary Bladder Neoplasms - metabolism Urinary Bladder Neoplasms - mortality Urinary Bladder Neoplasms - pathology Xenograft Model Antitumor Assays |
title | High PRMT5 expression is associated with poor overall survival and tumor progression in bladder cancer |
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