The miR-130 family promotes cell migration and invasion in bladder cancer through FAK and Akt phosphorylation by regulating PTEN
Bladder cancer causes an estimated 150,000 deaths per year worldwide. Although 15% of the recurrent bladder cancer becomes an invasive type, currently used targeted therapy for malignant bladder cancer is still not efficient. We focused on the miR-130 family (miR-130b, miR-301a and miR-301b) that wa...
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| Veröffentlicht in: | Scientific reports 2016-02, Vol.6 (1), p.20574-20574, Article 20574 |
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| creator | Egawa, Hiroshi Jingushi, Kentaro Hirono, Takayuki Ueda, Yuko Kitae, Kaori Nakata, Wataru Fujita, Kazutoshi Uemura, Motohide Nonomura, Norio Tsujikawa, Kazutake |
| description | Bladder cancer causes an estimated 150,000 deaths per year worldwide. Although 15% of the recurrent bladder cancer becomes an invasive type, currently used targeted therapy for malignant bladder cancer is still not efficient. We focused on the miR-130 family (miR-130b, miR-301a and miR-301b) that was significantly upregulated in bladder cancer specimens than that of the normal urothelial specimens. We analyzed the functional significance of miR-130 family using a 5637 bladder cancer cell line and revealed that miR-130 family of inhibitors suppressed cell migration and invasion by downregulating focal adhesion kinase (FAK) and Akt phosphorylation. Mechanistic analyses indicate that the miR-130 family directly targets phosphatase and tensin homolog deleted from chromosome 10 (PTEN), resulting in the upregulation of FAK and Akt phosphorylation. In clinical bladder cancer specimens, downregulation of PTEN was found to be closely correlated with miR-130 family expression levels. Overall, the miR-130 family has a crucial role in malignant progression of bladder cancer and thus the miR-130 family could be a promising therapeutic target for invasive bladder cancer. |
| doi_str_mv | 10.1038/srep20574 |
| format | Article |
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Although 15% of the recurrent bladder cancer becomes an invasive type, currently used targeted therapy for malignant bladder cancer is still not efficient. We focused on the miR-130 family (miR-130b, miR-301a and miR-301b) that was significantly upregulated in bladder cancer specimens than that of the normal urothelial specimens. We analyzed the functional significance of miR-130 family using a 5637 bladder cancer cell line and revealed that miR-130 family of inhibitors suppressed cell migration and invasion by downregulating focal adhesion kinase (FAK) and Akt phosphorylation. Mechanistic analyses indicate that the miR-130 family directly targets phosphatase and tensin homolog deleted from chromosome 10 (PTEN), resulting in the upregulation of FAK and Akt phosphorylation. In clinical bladder cancer specimens, downregulation of PTEN was found to be closely correlated with miR-130 family expression levels. Overall, the miR-130 family has a crucial role in malignant progression of bladder cancer and thus the miR-130 family could be a promising therapeutic target for invasive bladder cancer.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep20574</identifier><identifier>PMID: 26837847</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/109 ; 14/63 ; 3' Untranslated Regions ; 631/337/384/331 ; 692/4025/1334 ; 82/51 ; Aged ; Aged, 80 and over ; AKT protein ; Bladder cancer ; Cancer ; Cell adhesion & migration ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Chromosome 10 ; Female ; Focal adhesion kinase ; Focal Adhesion Kinase 1 - metabolism ; Gene Expression Regulation, Neoplastic ; Humanities and Social Sciences ; Humans ; Invasiveness ; Male ; MicroRNAs - genetics ; Middle Aged ; multidisciplinary ; Neoplasm Invasiveness ; Phosphorylation ; Proto-Oncogene Proteins c-akt - metabolism ; PTEN Phosphohydrolase - genetics ; PTEN Phosphohydrolase - metabolism ; PTEN protein ; Science ; Tensin ; Urinary bladder ; Urinary Bladder Neoplasms - genetics ; Urinary Bladder Neoplasms - metabolism ; Urinary Bladder Neoplasms - pathology</subject><ispartof>Scientific reports, 2016-02, Vol.6 (1), p.20574-20574, Article 20574</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Feb 2016</rights><rights>Copyright © 2016, Macmillan Publishers Limited 2016 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-c539fe116dc95687cc106b26497470d61fd6bb5bc6e377832902fdc2ec78dda53</citedby><cites>FETCH-LOGICAL-c504t-c539fe116dc95687cc106b26497470d61fd6bb5bc6e377832902fdc2ec78dda53</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/PMC4738343/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4738343/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26837847$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Egawa, Hiroshi</creatorcontrib><creatorcontrib>Jingushi, Kentaro</creatorcontrib><creatorcontrib>Hirono, Takayuki</creatorcontrib><creatorcontrib>Ueda, Yuko</creatorcontrib><creatorcontrib>Kitae, Kaori</creatorcontrib><creatorcontrib>Nakata, Wataru</creatorcontrib><creatorcontrib>Fujita, Kazutoshi</creatorcontrib><creatorcontrib>Uemura, Motohide</creatorcontrib><creatorcontrib>Nonomura, Norio</creatorcontrib><creatorcontrib>Tsujikawa, Kazutake</creatorcontrib><title>The miR-130 family promotes cell migration and invasion in bladder cancer through FAK and Akt phosphorylation by regulating PTEN</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Bladder cancer causes an estimated 150,000 deaths per year worldwide. Although 15% of the recurrent bladder cancer becomes an invasive type, currently used targeted therapy for malignant bladder cancer is still not efficient. We focused on the miR-130 family (miR-130b, miR-301a and miR-301b) that was significantly upregulated in bladder cancer specimens than that of the normal urothelial specimens. We analyzed the functional significance of miR-130 family using a 5637 bladder cancer cell line and revealed that miR-130 family of inhibitors suppressed cell migration and invasion by downregulating focal adhesion kinase (FAK) and Akt phosphorylation. Mechanistic analyses indicate that the miR-130 family directly targets phosphatase and tensin homolog deleted from chromosome 10 (PTEN), resulting in the upregulation of FAK and Akt phosphorylation. In clinical bladder cancer specimens, downregulation of PTEN was found to be closely correlated with miR-130 family expression levels. Overall, the miR-130 family has a crucial role in malignant progression of bladder cancer and thus the miR-130 family could be a promising therapeutic target for invasive bladder cancer.</description><subject>13/109</subject><subject>14/63</subject><subject>3' Untranslated Regions</subject><subject>631/337/384/331</subject><subject>692/4025/1334</subject><subject>82/51</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>AKT protein</subject><subject>Bladder cancer</subject><subject>Cancer</subject><subject>Cell adhesion & migration</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Chromosome 10</subject><subject>Female</subject><subject>Focal adhesion kinase</subject><subject>Focal Adhesion Kinase 1 - metabolism</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Invasiveness</subject><subject>Male</subject><subject>MicroRNAs - 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metabolism</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Invasiveness</topic><topic>Male</topic><topic>MicroRNAs - genetics</topic><topic>Middle Aged</topic><topic>multidisciplinary</topic><topic>Neoplasm Invasiveness</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>PTEN protein</topic><topic>Science</topic><topic>Tensin</topic><topic>Urinary bladder</topic><topic>Urinary Bladder Neoplasms - genetics</topic><topic>Urinary Bladder Neoplasms - metabolism</topic><topic>Urinary Bladder Neoplasms - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Egawa, Hiroshi</creatorcontrib><creatorcontrib>Jingushi, Kentaro</creatorcontrib><creatorcontrib>Hirono, Takayuki</creatorcontrib><creatorcontrib>Ueda, Yuko</creatorcontrib><creatorcontrib>Kitae, Kaori</creatorcontrib><creatorcontrib>Nakata, Wataru</creatorcontrib><creatorcontrib>Fujita, Kazutoshi</creatorcontrib><creatorcontrib>Uemura, Motohide</creatorcontrib><creatorcontrib>Nonomura, Norio</creatorcontrib><creatorcontrib>Tsujikawa, Kazutake</creatorcontrib><collection>Springer Nature OA Free Journals</collection><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>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content 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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Egawa, Hiroshi</au><au>Jingushi, Kentaro</au><au>Hirono, Takayuki</au><au>Ueda, Yuko</au><au>Kitae, Kaori</au><au>Nakata, Wataru</au><au>Fujita, Kazutoshi</au><au>Uemura, Motohide</au><au>Nonomura, Norio</au><au>Tsujikawa, Kazutake</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The miR-130 family promotes cell migration and invasion in bladder cancer through FAK and Akt phosphorylation by regulating PTEN</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2016-02-03</date><risdate>2016</risdate><volume>6</volume><issue>1</issue><spage>20574</spage><epage>20574</epage><pages>20574-20574</pages><artnum>20574</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Bladder cancer causes an estimated 150,000 deaths per year worldwide. Although 15% of the recurrent bladder cancer becomes an invasive type, currently used targeted therapy for malignant bladder cancer is still not efficient. We focused on the miR-130 family (miR-130b, miR-301a and miR-301b) that was significantly upregulated in bladder cancer specimens than that of the normal urothelial specimens. We analyzed the functional significance of miR-130 family using a 5637 bladder cancer cell line and revealed that miR-130 family of inhibitors suppressed cell migration and invasion by downregulating focal adhesion kinase (FAK) and Akt phosphorylation. Mechanistic analyses indicate that the miR-130 family directly targets phosphatase and tensin homolog deleted from chromosome 10 (PTEN), resulting in the upregulation of FAK and Akt phosphorylation. In clinical bladder cancer specimens, downregulation of PTEN was found to be closely correlated with miR-130 family expression levels. Overall, the miR-130 family has a crucial role in malignant progression of bladder cancer and thus the miR-130 family could be a promising therapeutic target for invasive bladder cancer.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26837847</pmid><doi>10.1038/srep20574</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/109 14/63 3' Untranslated Regions 631/337/384/331 692/4025/1334 82/51 Aged Aged, 80 and over AKT protein Bladder cancer Cancer Cell adhesion & migration Cell Line, Tumor Cell migration Cell Movement Chromosome 10 Female Focal adhesion kinase Focal Adhesion Kinase 1 - metabolism Gene Expression Regulation, Neoplastic Humanities and Social Sciences Humans Invasiveness Male MicroRNAs - genetics Middle Aged multidisciplinary Neoplasm Invasiveness Phosphorylation Proto-Oncogene Proteins c-akt - metabolism PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - metabolism PTEN protein Science Tensin Urinary bladder Urinary Bladder Neoplasms - genetics Urinary Bladder Neoplasms - metabolism Urinary Bladder Neoplasms - pathology |
| title | The miR-130 family promotes cell migration and invasion in bladder cancer through FAK and Akt phosphorylation by regulating PTEN |
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