Exploration of bladder cancer molecular mechanisms based on miRNA-mRNA regulatory network
To explore the complex molecular mechanisms of bladder cancer, mRNA and miRNA expression profiles were combined for systematic analyses. A total of 18 common differentially expressed genes (DEGs) were identified from two mRNA expression datasets which consisted of 206 tumor and 74 normal tissues. Th...
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| Veröffentlicht in: | Oncology reports 2017-03, Vol.37 (3), p.1461-1468 |
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| container_title | Oncology reports |
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| creator | Li, Wenfeng Liu, Jia Zou, Di Cai, Xiaye Wang, Jingying Wang, Jinmeng Zhu, Li Zhao, Liang Ou, Rongying Xu, Yunsheng |
| description | To explore the complex molecular mechanisms of bladder cancer, mRNA and miRNA expression profiles were combined for systematic analyses. A total of 18 common differentially expressed genes (DEGs) were identified from two mRNA expression datasets which consisted of 206 tumor and 74 normal tissues. Then, survival analysis based on the SurvExpress database showed that the common DEGs were able to significantly differentiate low- and high-risk groups in 4 public bladder cancer datasets (p |
| doi_str_mv | 10.3892/or.2017.5433 |
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A total of 18 common differentially expressed genes (DEGs) were identified from two mRNA expression datasets which consisted of 206 tumor and 74 normal tissues. Then, survival analysis based on the SurvExpress database showed that the common DEGs were able to significantly differentiate low- and high-risk groups in 4 public bladder cancer datasets (p<0.01). Notably, the tumor and normal samples were able to be almost clearly classified into 4 groups based on these identified common DEGs. In addition, 6 out of the 18 common DEGs, including ALDH1A1 and SRPX, are regulated by 6 reported miRNAs based on regulatory network analyses. Expression levels of the 6 DEGs were validated in 10 bladder cancer samples using RT-PCR, and the expression values were concordant with the microarray results. Collectively, our analyses indicated that various biological processes are involved in the development and progression of bladder cancer. Firstly, cell cycle checkpoints and DNA repair networks of cancer stem-like cells were regulated by high expression of ALDH1A1, and hence promoted tumor self-renewal or metastasis. Then, activation of HspB6 induced the angiogenesis process which provides necessary nutrition and oxygen for tumor cells. Moreover, downregulation of the expression of tumor-suppressor genes SRPX and FLNC further promoted apoptosis and metastasis. The identification of potential biological processes and genes can be helpful for the understanding of bladder cancer molecular mechanisms.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2017.5433</identifier><identifier>PMID: 28184944</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Aldehyde Dehydrogenase - genetics ; Analysis ; Angiogenesis ; Bladder cancer ; Care and treatment ; Cell cycle ; Datasets ; Development and progression ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Genetic aspects ; Health aspects ; Humans ; Kinases ; Messenger RNA ; Metastasis ; MicroRNA ; MicroRNAs - genetics ; Ontology ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; Studies ; Urinary Bladder Neoplasms - genetics ; Urinary Bladder Neoplasms - pathology</subject><ispartof>Oncology reports, 2017-03, Vol.37 (3), p.1461-1468</ispartof><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c521t-cb37e3525b1d846d524d7782486fe2c1d60401317c16377562ebce8c99c9c5f43</citedby><cites>FETCH-LOGICAL-c521t-cb37e3525b1d846d524d7782486fe2c1d60401317c16377562ebce8c99c9c5f43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28184944$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Wenfeng</creatorcontrib><creatorcontrib>Liu, Jia</creatorcontrib><creatorcontrib>Zou, Di</creatorcontrib><creatorcontrib>Cai, Xiaye</creatorcontrib><creatorcontrib>Wang, Jingying</creatorcontrib><creatorcontrib>Wang, Jinmeng</creatorcontrib><creatorcontrib>Zhu, Li</creatorcontrib><creatorcontrib>Zhao, Liang</creatorcontrib><creatorcontrib>Ou, Rongying</creatorcontrib><creatorcontrib>Xu, Yunsheng</creatorcontrib><title>Exploration of bladder cancer molecular mechanisms based on miRNA-mRNA regulatory network</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>To explore the complex molecular mechanisms of bladder cancer, mRNA and miRNA expression profiles were combined for systematic analyses. A total of 18 common differentially expressed genes (DEGs) were identified from two mRNA expression datasets which consisted of 206 tumor and 74 normal tissues. Then, survival analysis based on the SurvExpress database showed that the common DEGs were able to significantly differentiate low- and high-risk groups in 4 public bladder cancer datasets (p<0.01). Notably, the tumor and normal samples were able to be almost clearly classified into 4 groups based on these identified common DEGs. In addition, 6 out of the 18 common DEGs, including ALDH1A1 and SRPX, are regulated by 6 reported miRNAs based on regulatory network analyses. Expression levels of the 6 DEGs were validated in 10 bladder cancer samples using RT-PCR, and the expression values were concordant with the microarray results. Collectively, our analyses indicated that various biological processes are involved in the development and progression of bladder cancer. Firstly, cell cycle checkpoints and DNA repair networks of cancer stem-like cells were regulated by high expression of ALDH1A1, and hence promoted tumor self-renewal or metastasis. Then, activation of HspB6 induced the angiogenesis process which provides necessary nutrition and oxygen for tumor cells. Moreover, downregulation of the expression of tumor-suppressor genes SRPX and FLNC further promoted apoptosis and metastasis. The identification of potential biological processes and genes can be helpful for the understanding of bladder cancer molecular mechanisms.</description><subject>Aldehyde Dehydrogenase - genetics</subject><subject>Analysis</subject><subject>Angiogenesis</subject><subject>Bladder cancer</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Datasets</subject><subject>Development and progression</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Regulatory Networks</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Kinases</subject><subject>Messenger RNA</subject><subject>Metastasis</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>Ontology</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Studies</subject><subject>Urinary Bladder Neoplasms - genetics</subject><subject>Urinary Bladder Neoplasms - pathology</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpt0c1rFTEQAPAgFlurN8-yIIgH95nJxyY5PkqrQqkgCnoK2exs39bs5pnsUvvfm6X1oyKBzBB-MyQZQp4B3XBt2JuYNoyC2kjB-QNyBMpAzQSHhyWnDGrO5ZdD8jjnK0qZoo15RA6ZBi2MEEfk6-mPfYjJzUOcqthXbXBdh6nybvIljDGgX4IrGfqdm4Y85qp1Gbuq-HH4eLGtx7JVCS8Lm2O6qSacr2P69oQc9C5kfHoXj8nns9NPJ-_q8w9v359sz2svGcy1b7lCLplsodOi6SQTnVKaCd30yDx0DRUUOCgPDVdKNgxbj9ob442XveDH5NVt332K3xfMsx2H7DEEN2FcsgXdKCmk0rzQF__Qq7ikqdzOghHADNVK_FGXLqAdpj7Oyfm1qd0KA8BNI1hRm_-osjocBx8n7Idyfq_g5V8FO3Rh3uUYlvXn8334-hb6FHNO2Nt9GkaXbixQu47cxmTXkdt15IU_v3vU0o7Y_ca_Zsx_ArojoxE</recordid><startdate>20170301</startdate><enddate>20170301</enddate><creator>Li, Wenfeng</creator><creator>Liu, Jia</creator><creator>Zou, Di</creator><creator>Cai, Xiaye</creator><creator>Wang, Jingying</creator><creator>Wang, Jinmeng</creator><creator>Zhu, Li</creator><creator>Zhao, Liang</creator><creator>Ou, Rongying</creator><creator>Xu, Yunsheng</creator><general>Spandidos Publications</general><general>Spandidos Publications UK 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>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20170301</creationdate><title>Exploration of bladder cancer molecular mechanisms based on miRNA-mRNA regulatory network</title><author>Li, Wenfeng ; Liu, Jia ; Zou, Di ; Cai, Xiaye ; Wang, Jingying ; Wang, Jinmeng ; Zhu, Li ; Zhao, Liang ; Ou, Rongying ; Xu, Yunsheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c521t-cb37e3525b1d846d524d7782486fe2c1d60401317c16377562ebce8c99c9c5f43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Aldehyde Dehydrogenase - genetics</topic><topic>Analysis</topic><topic>Angiogenesis</topic><topic>Bladder cancer</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Datasets</topic><topic>Development and progression</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Regulatory Networks</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Kinases</topic><topic>Messenger RNA</topic><topic>Metastasis</topic><topic>MicroRNA</topic><topic>MicroRNAs - genetics</topic><topic>Ontology</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Studies</topic><topic>Urinary Bladder Neoplasms - genetics</topic><topic>Urinary Bladder Neoplasms - pathology</topic><toplevel>online_resources</toplevel><creatorcontrib>Li, Wenfeng</creatorcontrib><creatorcontrib>Liu, Jia</creatorcontrib><creatorcontrib>Zou, Di</creatorcontrib><creatorcontrib>Cai, Xiaye</creatorcontrib><creatorcontrib>Wang, Jingying</creatorcontrib><creatorcontrib>Wang, Jinmeng</creatorcontrib><creatorcontrib>Zhu, Li</creatorcontrib><creatorcontrib>Zhao, Liang</creatorcontrib><creatorcontrib>Ou, Rongying</creatorcontrib><creatorcontrib>Xu, Yunsheng</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>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>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Wenfeng</au><au>Liu, Jia</au><au>Zou, Di</au><au>Cai, Xiaye</au><au>Wang, Jingying</au><au>Wang, Jinmeng</au><au>Zhu, Li</au><au>Zhao, Liang</au><au>Ou, Rongying</au><au>Xu, Yunsheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exploration of bladder cancer molecular mechanisms based on miRNA-mRNA regulatory network</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2017-03-01</date><risdate>2017</risdate><volume>37</volume><issue>3</issue><spage>1461</spage><epage>1468</epage><pages>1461-1468</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>To explore the complex molecular mechanisms of bladder cancer, mRNA and miRNA expression profiles were combined for systematic analyses. A total of 18 common differentially expressed genes (DEGs) were identified from two mRNA expression datasets which consisted of 206 tumor and 74 normal tissues. Then, survival analysis based on the SurvExpress database showed that the common DEGs were able to significantly differentiate low- and high-risk groups in 4 public bladder cancer datasets (p<0.01). Notably, the tumor and normal samples were able to be almost clearly classified into 4 groups based on these identified common DEGs. In addition, 6 out of the 18 common DEGs, including ALDH1A1 and SRPX, are regulated by 6 reported miRNAs based on regulatory network analyses. Expression levels of the 6 DEGs were validated in 10 bladder cancer samples using RT-PCR, and the expression values were concordant with the microarray results. Collectively, our analyses indicated that various biological processes are involved in the development and progression of bladder cancer. Firstly, cell cycle checkpoints and DNA repair networks of cancer stem-like cells were regulated by high expression of ALDH1A1, and hence promoted tumor self-renewal or metastasis. Then, activation of HspB6 induced the angiogenesis process which provides necessary nutrition and oxygen for tumor cells. Moreover, downregulation of the expression of tumor-suppressor genes SRPX and FLNC further promoted apoptosis and metastasis. The identification of potential biological processes and genes can be helpful for the understanding of bladder cancer molecular mechanisms.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>28184944</pmid><doi>10.3892/or.2017.5433</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncology reports, 2017-03, Vol.37 (3), p.1461-1468 |
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| language | eng |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Aldehyde Dehydrogenase - genetics Analysis Angiogenesis Bladder cancer Care and treatment Cell cycle Datasets Development and progression Gene expression Gene Expression Profiling Gene Expression Regulation, Neoplastic Gene Regulatory Networks Genetic aspects Health aspects Humans Kinases Messenger RNA Metastasis MicroRNA MicroRNAs - genetics Ontology Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Studies Urinary Bladder Neoplasms - genetics Urinary Bladder Neoplasms - pathology |
| title | Exploration of bladder cancer molecular mechanisms based on miRNA-mRNA regulatory network |
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