miR-301a promotes pancreatic cancer cell proliferation by directly inhibiting bim expression
It is well known that microRNAs (miRNAs) play an important role in many diseases, including tumorigenesis. However, the mechanisms by which miRNAs regulate pancreatic cancer (PC) development remain poorly understood. In the present study, we assayed expression level of miR‐301a in PC tissues by real...
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| Veröffentlicht in: | Journal of cellular biochemistry 2012-10, Vol.113 (10), p.3229-3235 |
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| creator | Chen, Zhen Chen, Lian-Yu Dai, Hai-Yan Wang, Peng Gao, Song Wang, Kun |
| description | It is well known that microRNAs (miRNAs) play an important role in many diseases, including tumorigenesis. However, the mechanisms by which miRNAs regulate pancreatic cancer (PC) development remain poorly understood. In the present study, we assayed expression level of miR‐301a in PC tissues by real‐time PCR, and defined the target gene and biological function by luciferase reporter assay and Western blot analysis. We first verified that the expression level of miR‐301a was significantly increased in PC tissues. Moreover, miR‐301a overexpression promoted PC cell proliferation, whereas its depletion decreased cell proliferation. We further demonstrated that miR‐301a directly targeted 3′‐UTR of Bim gene, and inhibited its protein expression in vitro and in vivo. Importantly, Bim re‐expression reduced PC cell proliferation induced by miR‐301a. These data suggest an important role of miR‐301a in the molecular etiology of PC and implicate the potential application of miR‐301a in PC therapy. J. Cell. Biochem. 113: 3229–3235, 2012. © 2012 Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/jcb.24200 |
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However, the mechanisms by which miRNAs regulate pancreatic cancer (PC) development remain poorly understood. In the present study, we assayed expression level of miR‐301a in PC tissues by real‐time PCR, and defined the target gene and biological function by luciferase reporter assay and Western blot analysis. We first verified that the expression level of miR‐301a was significantly increased in PC tissues. Moreover, miR‐301a overexpression promoted PC cell proliferation, whereas its depletion decreased cell proliferation. We further demonstrated that miR‐301a directly targeted 3′‐UTR of Bim gene, and inhibited its protein expression in vitro and in vivo. Importantly, Bim re‐expression reduced PC cell proliferation induced by miR‐301a. These data suggest an important role of miR‐301a in the molecular etiology of PC and implicate the potential application of miR‐301a in PC therapy. J. Cell. Biochem. 113: 3229–3235, 2012. © 2012 Wiley Periodicals, Inc.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.24200</identifier><identifier>PMID: 22628193</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>3' Untranslated Regions ; Adult ; Aged ; APOPTOSIS ; Apoptosis Regulatory Proteins - genetics ; Apoptosis Regulatory Proteins - metabolism ; Bcl-2-Like Protein 11 ; Bim ; Blotting, Western ; Cell Proliferation ; Female ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Humans ; Luciferases - metabolism ; Male ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Middle Aged ; miR-301a ; PANCREATIC CANCER ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; PROLIFERATION ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - metabolism ; Real-Time Polymerase Chain Reaction ; RNA, Neoplasm - genetics ; RNA, Neoplasm - metabolism</subject><ispartof>Journal of cellular biochemistry, 2012-10, Vol.113 (10), p.3229-3235</ispartof><rights>Copyright © 2012 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4290-17a3a60c13e0aca859acd4b4019410fab4fbf9fb6608912720a2f14d371854e73</citedby><cites>FETCH-LOGICAL-c4290-17a3a60c13e0aca859acd4b4019410fab4fbf9fb6608912720a2f14d371854e73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.24200$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.24200$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27922,27923,45572,45573</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22628193$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Zhen</creatorcontrib><creatorcontrib>Chen, Lian-Yu</creatorcontrib><creatorcontrib>Dai, Hai-Yan</creatorcontrib><creatorcontrib>Wang, Peng</creatorcontrib><creatorcontrib>Gao, Song</creatorcontrib><creatorcontrib>Wang, Kun</creatorcontrib><title>miR-301a promotes pancreatic cancer cell proliferation by directly inhibiting bim expression</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem</addtitle><description>It is well known that microRNAs (miRNAs) play an important role in many diseases, including tumorigenesis. However, the mechanisms by which miRNAs regulate pancreatic cancer (PC) development remain poorly understood. In the present study, we assayed expression level of miR‐301a in PC tissues by real‐time PCR, and defined the target gene and biological function by luciferase reporter assay and Western blot analysis. We first verified that the expression level of miR‐301a was significantly increased in PC tissues. Moreover, miR‐301a overexpression promoted PC cell proliferation, whereas its depletion decreased cell proliferation. We further demonstrated that miR‐301a directly targeted 3′‐UTR of Bim gene, and inhibited its protein expression in vitro and in vivo. Importantly, Bim re‐expression reduced PC cell proliferation induced by miR‐301a. These data suggest an important role of miR‐301a in the molecular etiology of PC and implicate the potential application of miR‐301a in PC therapy. J. Cell. Biochem. 113: 3229–3235, 2012. © 2012 Wiley Periodicals, Inc.</description><subject>3' Untranslated Regions</subject><subject>Adult</subject><subject>Aged</subject><subject>APOPTOSIS</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Bcl-2-Like Protein 11</subject><subject>Bim</subject><subject>Blotting, Western</subject><subject>Cell Proliferation</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Luciferases - metabolism</subject><subject>Male</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>miR-301a</subject><subject>PANCREATIC CANCER</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>PROLIFERATION</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>RNA, Neoplasm - genetics</subject><subject>RNA, Neoplasm - metabolism</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEtPGzEUha2qqKQpi_4B5CUsBq4fGY-XEFFKFIGEWrFBsmznTnGYR7Angvz7Og1h19W90vnO0dEh5DuDMwbAz5fenXHJAT6REQOtCllK-ZmMQAkouGD8kHxNaQkAWgv-hRxyXvKKaTEij224LwQwS1exb_sBE13Zzke0Q_DU5xcj9dg0W70JNcYs9B11G7oIEf3QbGjonoILQ-j-UBdaim-riCll6hs5qG2T8Oj9jsnvH1e_pj-L-d31zfRiXnjJNRRMWWFL8EwgWG-ribZ-IZ0EpiWD2jpZu1rXriyh0owrDpbXTC6EYtVEohJjcrLLzR1f1pgG04a0LW077NfJMBBCTpTULKOnO9THPqWItVnF0Nq4yZDZjmnymObfmJk9fo9duxYXH-R-vQyc74DX0ODm_0lmNr3cRxY7R0gDvn04bHw2pRJqYh5ur01VzsS9fpibSvwF2FiMqw</recordid><startdate>201210</startdate><enddate>201210</enddate><creator>Chen, Zhen</creator><creator>Chen, Lian-Yu</creator><creator>Dai, Hai-Yan</creator><creator>Wang, Peng</creator><creator>Gao, Song</creator><creator>Wang, Kun</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</scope><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></search><sort><creationdate>201210</creationdate><title>miR-301a promotes pancreatic cancer cell proliferation by directly inhibiting bim expression</title><author>Chen, Zhen ; Chen, Lian-Yu ; Dai, Hai-Yan ; Wang, Peng ; Gao, Song ; Wang, Kun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4290-17a3a60c13e0aca859acd4b4019410fab4fbf9fb6608912720a2f14d371854e73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>3' Untranslated Regions</topic><topic>Adult</topic><topic>Aged</topic><topic>APOPTOSIS</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Bcl-2-Like Protein 11</topic><topic>Bim</topic><topic>Blotting, Western</topic><topic>Cell Proliferation</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Luciferases - metabolism</topic><topic>Male</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>miR-301a</topic><topic>PANCREATIC CANCER</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>PROLIFERATION</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>RNA, Neoplasm - genetics</topic><topic>RNA, Neoplasm - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Zhen</creatorcontrib><creatorcontrib>Chen, Lian-Yu</creatorcontrib><creatorcontrib>Dai, Hai-Yan</creatorcontrib><creatorcontrib>Wang, Peng</creatorcontrib><creatorcontrib>Gao, Song</creatorcontrib><creatorcontrib>Wang, Kun</creatorcontrib><collection>Istex</collection><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>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Zhen</au><au>Chen, Lian-Yu</au><au>Dai, Hai-Yan</au><au>Wang, Peng</au><au>Gao, Song</au><au>Wang, Kun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-301a promotes pancreatic cancer cell proliferation by directly inhibiting bim expression</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J. Cell. Biochem</addtitle><date>2012-10</date><risdate>2012</risdate><volume>113</volume><issue>10</issue><spage>3229</spage><epage>3235</epage><pages>3229-3235</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>It is well known that microRNAs (miRNAs) play an important role in many diseases, including tumorigenesis. However, the mechanisms by which miRNAs regulate pancreatic cancer (PC) development remain poorly understood. In the present study, we assayed expression level of miR‐301a in PC tissues by real‐time PCR, and defined the target gene and biological function by luciferase reporter assay and Western blot analysis. We first verified that the expression level of miR‐301a was significantly increased in PC tissues. Moreover, miR‐301a overexpression promoted PC cell proliferation, whereas its depletion decreased cell proliferation. We further demonstrated that miR‐301a directly targeted 3′‐UTR of Bim gene, and inhibited its protein expression in vitro and in vivo. Importantly, Bim re‐expression reduced PC cell proliferation induced by miR‐301a. These data suggest an important role of miR‐301a in the molecular etiology of PC and implicate the potential application of miR‐301a in PC therapy. J. Cell. Biochem. 113: 3229–3235, 2012. © 2012 Wiley Periodicals, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>22628193</pmid><doi>10.1002/jcb.24200</doi><tpages>7</tpages></addata></record> |
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| subjects | 3' Untranslated Regions Adult Aged APOPTOSIS Apoptosis Regulatory Proteins - genetics Apoptosis Regulatory Proteins - metabolism Bcl-2-Like Protein 11 Bim Blotting, Western Cell Proliferation Female Gene Expression Regulation, Neoplastic HEK293 Cells Humans Luciferases - metabolism Male Membrane Proteins - genetics Membrane Proteins - metabolism MicroRNAs - genetics MicroRNAs - metabolism Middle Aged miR-301a PANCREATIC CANCER Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology PROLIFERATION Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Real-Time Polymerase Chain Reaction RNA, Neoplasm - genetics RNA, Neoplasm - metabolism |
| title | miR-301a promotes pancreatic cancer cell proliferation by directly inhibiting bim expression |
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