MiR-133b regulates bladder cancer cell proliferation and apoptosis by targeting Bcl-w and Akt1

MiR-133b is a muscle-specific microRNA; it has a role in the formation of cardiocytes and the expression of myocardium ion channels by regulating target genes. Many human malignant tumors demonstrate a low expression of miR-133b, as noted in colorectal, lung, esophagus and bladder cancers, but the r...

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Published in:Cancer cell international 2014-07, Vol.14 (1), p.70-70, Article 70
Main Authors: Chen, Xiao-Nan, Wang, Ke-Feng, Xu, Zhen-Qun, Li, Shi-Jie, Liu, Qiang, Fu, Dong-Hui, Wang, Xia, Wu, Bin
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Language:English
Subjects:
Apoptosis
Bladder cancer
Cell growth
Flow cytometry
Gene expression
Kinases
Medical research
MicroRNAs
Molecular weight
Primary Research
Proteins
Rodents
Software
Statistical analysis
Studies
Tumors
Variance analysis
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description MiR-133b is a muscle-specific microRNA; it has a role in the formation of cardiocytes and the expression of myocardium ion channels by regulating target genes. Many human malignant tumors demonstrate a low expression of miR-133b, as noted in colorectal, lung, esophagus and bladder cancers, but the role of miR-133b in bladder cancer is unknown. The expression of miR-133b in clinical bladder cancer specimens and adjacent normal tissues was confirmed by stem-loop RT-PCR. We also analyzed the relationship between miR-133b expression and clinicopathological factors of bladder cancer. Bcl-w and Akt1 protein expression in 41 bladder cancer specimens and adjacent normal tissues was detected by Western blot. After transfection of miR-133b mimics or inhibitor into a T24 human bladder cancer cell line, Bcl-w and Akt1 protein and mRNA expression were examined by Western blot and RT-PCR, respectively. The effect of miR-133b on T24 cell proliferation and apoptosis was measured by CCK-8 tests and flow cytometry, respectively. The expression of miR-133b in bladder cancer tissues from 41 patients was significantly down-regulated (P 
doi_str_mv 10.1186/s12935-014-0070-3
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Many human malignant tumors demonstrate a low expression of miR-133b, as noted in colorectal, lung, esophagus and bladder cancers, but the role of miR-133b in bladder cancer is unknown. The expression of miR-133b in clinical bladder cancer specimens and adjacent normal tissues was confirmed by stem-loop RT-PCR. We also analyzed the relationship between miR-133b expression and clinicopathological factors of bladder cancer. Bcl-w and Akt1 protein expression in 41 bladder cancer specimens and adjacent normal tissues was detected by Western blot. After transfection of miR-133b mimics or inhibitor into a T24 human bladder cancer cell line, Bcl-w and Akt1 protein and mRNA expression were examined by Western blot and RT-PCR, respectively. The effect of miR-133b on T24 cell proliferation and apoptosis was measured by CCK-8 tests and flow cytometry, respectively. The expression of miR-133b in bladder cancer tissues from 41 patients was significantly down-regulated (P < 0.01); low expression of miR-133b was strongly associated with high-grade bladder cancer (P < 0.01). Bcl-w and Akt1 proteins were significantly overexpressed in bladder cancer tissues versus adjacent normal tissues (P < 0.01 for both). The expression of Akt1 and Bcl-w proteins and Akt1 mRNA, in T24 cells was significantly down-regulated or up-regulated after transfection of miR-133b mimics or inhibitor, respectively; however, there was no significant difference in Bcl-w mRNA expression. Transfection of HEK-293 T cells with miR-133b significantly suppressed a luciferase-reporter containing the Bcl-w or Akt 1 3'-untranslated regions. MiR-133b mimics significantly inhibited T24 cell proliferation, as well as increased T24 cell apoptosis (P < 0.05 and P < 0.01, respectively) while the miR-133b inhibitor increased and decreased these, respectively (P < 0.05 for both). MiR-133b may play a very important role in the proliferation and apoptosis of T24 cells by regulating the expression of Bcl-w and Akt1.]]></description><identifier>ISSN: 1475-2867</identifier><identifier>EISSN: 1475-2867</identifier><identifier>DOI: 10.1186/s12935-014-0070-3</identifier><identifier>PMID: 25414595</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Apoptosis ; Bladder cancer ; Cell growth ; Flow cytometry ; Gene expression ; Kinases ; Medical research ; MicroRNAs ; Molecular weight ; Primary Research ; Proteins ; Rodents ; Software ; Statistical analysis ; Studies ; Tumors ; Variance analysis</subject><ispartof>Cancer cell international, 2014-07, Vol.14 (1), p.70-70, Article 70</ispartof><rights>2014 Wu et al.; licensee Springer This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>Copyright © 2014 Wu et al.; licensee Springer 2014 Wu et al.; licensee Springer</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b589t-ea0a099091933acf0f850bb86f896111255e85a6877fc79011be378d60d7f9623</citedby><cites>FETCH-LOGICAL-b589t-ea0a099091933acf0f850bb86f896111255e85a6877fc79011be378d60d7f9623</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/PMC4238049/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1552153146?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25414595$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Xiao-Nan</creatorcontrib><creatorcontrib>Wang, Ke-Feng</creatorcontrib><creatorcontrib>Xu, Zhen-Qun</creatorcontrib><creatorcontrib>Li, Shi-Jie</creatorcontrib><creatorcontrib>Liu, Qiang</creatorcontrib><creatorcontrib>Fu, Dong-Hui</creatorcontrib><creatorcontrib>Wang, Xia</creatorcontrib><creatorcontrib>Wu, Bin</creatorcontrib><title>MiR-133b regulates bladder cancer cell proliferation and apoptosis by targeting Bcl-w and Akt1</title><title>Cancer cell international</title><addtitle>Cancer Cell Int</addtitle><description><![CDATA[MiR-133b is a muscle-specific microRNA; it has a role in the formation of cardiocytes and the expression of myocardium ion channels by regulating target genes. Many human malignant tumors demonstrate a low expression of miR-133b, as noted in colorectal, lung, esophagus and bladder cancers, but the role of miR-133b in bladder cancer is unknown. The expression of miR-133b in clinical bladder cancer specimens and adjacent normal tissues was confirmed by stem-loop RT-PCR. We also analyzed the relationship between miR-133b expression and clinicopathological factors of bladder cancer. Bcl-w and Akt1 protein expression in 41 bladder cancer specimens and adjacent normal tissues was detected by Western blot. After transfection of miR-133b mimics or inhibitor into a T24 human bladder cancer cell line, Bcl-w and Akt1 protein and mRNA expression were examined by Western blot and RT-PCR, respectively. The effect of miR-133b on T24 cell proliferation and apoptosis was measured by CCK-8 tests and flow cytometry, respectively. 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MiR-133b may play a very important role in the proliferation and apoptosis of T24 cells by regulating the expression of Bcl-w and Akt1.]]></description><subject>Apoptosis</subject><subject>Bladder cancer</subject><subject>Cell growth</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Kinases</subject><subject>Medical research</subject><subject>MicroRNAs</subject><subject>Molecular weight</subject><subject>Primary Research</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Software</subject><subject>Statistical analysis</subject><subject>Studies</subject><subject>Tumors</subject><subject>Variance analysis</subject><issn>1475-2867</issn><issn>1475-2867</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNp1kstq3TAURUVpaR7tB3QSDJ10ouQcy3pNCnknkFAo7bRCtuUbpb6WI8kN-fv45iYhKe3oCM7SZrMkQj4h7CIqsZew1IxTwIoCSKDsDdnESnJaKiHfvjhvkK2UrgFQKgHvyUbJK6y45pvk16X_TpGxuohuMfU2u1TUvW1bF4vGDs1quL4vxhh637losw9DYYe2sGMYc0h-5u-KbOPCZT8sioOmp7cPwP7vjB_Iu872yX18nNvk58nxj8MzevHt9Pxw_4LWXOlMnQULWoNGzZhtOugUh7pWolNaIGLJuVPcCiVl10gNiLVjUrUCWtlpUbJt8nWdO0710rWNG3K0vRmjX9p4Z4L15vVm8FdmEf6YqmQKKj0HHK0Dah_-E_B604SlWfs3s3-z8m_YHPPlsUcMN5NL2Sx9Wgm0gwtTMiiY5JxpJWf081_odZjiMFsyyHmJnGElZgrXVBNDStF1z5UQzOoT_LPEzksZzzeeXp3dA9nIrJI</recordid><startdate>20140719</startdate><enddate>20140719</enddate><creator>Chen, Xiao-Nan</creator><creator>Wang, Ke-Feng</creator><creator>Xu, Zhen-Qun</creator><creator>Li, Shi-Jie</creator><creator>Liu, Qiang</creator><creator>Fu, Dong-Hui</creator><creator>Wang, Xia</creator><creator>Wu, Bin</creator><general>BioMed Central</general><general>BioMed Central Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140719</creationdate><title>MiR-133b regulates bladder cancer cell proliferation and apoptosis by targeting Bcl-w and Akt1</title><author>Chen, Xiao-Nan ; 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it has a role in the formation of cardiocytes and the expression of myocardium ion channels by regulating target genes. Many human malignant tumors demonstrate a low expression of miR-133b, as noted in colorectal, lung, esophagus and bladder cancers, but the role of miR-133b in bladder cancer is unknown. The expression of miR-133b in clinical bladder cancer specimens and adjacent normal tissues was confirmed by stem-loop RT-PCR. We also analyzed the relationship between miR-133b expression and clinicopathological factors of bladder cancer. Bcl-w and Akt1 protein expression in 41 bladder cancer specimens and adjacent normal tissues was detected by Western blot. After transfection of miR-133b mimics or inhibitor into a T24 human bladder cancer cell line, Bcl-w and Akt1 protein and mRNA expression were examined by Western blot and RT-PCR, respectively. The effect of miR-133b on T24 cell proliferation and apoptosis was measured by CCK-8 tests and flow cytometry, respectively. The expression of miR-133b in bladder cancer tissues from 41 patients was significantly down-regulated (P < 0.01); low expression of miR-133b was strongly associated with high-grade bladder cancer (P < 0.01). Bcl-w and Akt1 proteins were significantly overexpressed in bladder cancer tissues versus adjacent normal tissues (P < 0.01 for both). The expression of Akt1 and Bcl-w proteins and Akt1 mRNA, in T24 cells was significantly down-regulated or up-regulated after transfection of miR-133b mimics or inhibitor, respectively; however, there was no significant difference in Bcl-w mRNA expression. Transfection of HEK-293 T cells with miR-133b significantly suppressed a luciferase-reporter containing the Bcl-w or Akt 1 3'-untranslated regions. MiR-133b mimics significantly inhibited T24 cell proliferation, as well as increased T24 cell apoptosis (P < 0.05 and P < 0.01, respectively) while the miR-133b inhibitor increased and decreased these, respectively (P < 0.05 for both). MiR-133b may play a very important role in the proliferation and apoptosis of T24 cells by regulating the expression of Bcl-w and Akt1.]]></abstract><cop>England</cop><pub>BioMed Central</pub><pmid>25414595</pmid><doi>10.1186/s12935-014-0070-3</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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subjects Apoptosis
Bladder cancer
Cell growth
Flow cytometry
Gene expression
Kinases
Medical research
MicroRNAs
Molecular weight
Primary Research
Proteins
Rodents
Software
Statistical analysis
Studies
Tumors
Variance analysis
title MiR-133b regulates bladder cancer cell proliferation and apoptosis by targeting Bcl-w and Akt1
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