Up-regulation of microRNA-1290 impairs cytokinesis and affects the reprogramming of colon cancer cells
► miR-1290 is up-regulated in colon cancer cells. ► Up-regulation of miR-1290 impairs cytokinesis. ► miR-1290 overexpression affects the reprogramming of colon cancer cells. Abnormal cytokinesis increases the possibility of nuclear fusion in tumor cells. However, the role of microRNAs (miRNAs) in ab...
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Veröffentlicht in: | Cancer letters 2013-02, Vol.329 (2), p.155-163 |
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description | ► miR-1290 is up-regulated in colon cancer cells. ► Up-regulation of miR-1290 impairs cytokinesis. ► miR-1290 overexpression affects the reprogramming of colon cancer cells.
Abnormal cytokinesis increases the possibility of nuclear fusion in tumor cells. However, the role of microRNAs (miRNAs) in abnormal cytokinesis is unclear. Here, we found that miR-1290 was significantly up-regulated in clinical colon cancer tissues. Up-regulation of miR-1290 postponed cytokinesis and led to the formation of multinucleated cells. KIF13B was a target of miR-1290 that was involved in aberrant cytokinesis. Furthermore, enforced expression of miR-1290 activated the Wnt pathway and increased the reprogramming-related transcript factors c-Myc and Nanog. Our results suggest that up-regulation of miR-1290 in colon cancer cells impaired cytokinesis and affected reprogramming. |
doi_str_mv | 10.1016/j.canlet.2012.10.038 |
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Abnormal cytokinesis increases the possibility of nuclear fusion in tumor cells. However, the role of microRNAs (miRNAs) in abnormal cytokinesis is unclear. Here, we found that miR-1290 was significantly up-regulated in clinical colon cancer tissues. Up-regulation of miR-1290 postponed cytokinesis and led to the formation of multinucleated cells. KIF13B was a target of miR-1290 that was involved in aberrant cytokinesis. Furthermore, enforced expression of miR-1290 activated the Wnt pathway and increased the reprogramming-related transcript factors c-Myc and Nanog. Our results suggest that up-regulation of miR-1290 in colon cancer cells impaired cytokinesis and affected reprogramming.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2012.10.038</identifier><identifier>PMID: 23142292</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Adenoma - genetics ; Adenoma - metabolism ; Adenoma - pathology ; Base Sequence ; Binding Sites ; Breast cancer ; Cell division ; Cell growth ; Cell Line, Tumor ; Cell Nucleus Division ; Cell Proliferation ; Chromosomes ; Colon cancer ; Colonic Neoplasms - genetics ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - pathology ; Colorectal cancer ; colorectal neoplasms ; Cytokinesis ; Cytokinesis - genetics ; gene expression regulation ; Gene Expression Regulation, Neoplastic ; Hematology, Oncology and Palliative Medicine ; Homeodomain Proteins - metabolism ; Humans ; Hybridization ; KIF13B ; Kinases ; Kinesin - genetics ; Kinesin - metabolism ; microRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; MicroRNAs - physiology ; miR-1290 ; Nanog Homeobox Protein ; NF-kappa B - metabolism ; Phosphatase ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Proto-Oncogene Proteins c-myc - metabolism ; RNA Interference ; Studies ; Transcription factors ; Transcription, Genetic ; Up-Regulation ; Wnt Signaling Pathway</subject><ispartof>Cancer letters, 2013-02, Vol.329 (2), p.155-163</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2012 Elsevier Ireland Ltd</rights><rights>Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.</rights><rights>Copyright Elsevier Limited Feb 28, 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c535t-f8f71a97022e7166d54930770ecccf53a8ff704c478258830911279928ca35d3</citedby><cites>FETCH-LOGICAL-c535t-f8f71a97022e7166d54930770ecccf53a8ff704c478258830911279928ca35d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S030438351200643X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23142292$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Jia</creatorcontrib><creatorcontrib>Ji, Xiaowei</creatorcontrib><creatorcontrib>Zhu, Linlin</creatorcontrib><creatorcontrib>Jiang, Qiaoli</creatorcontrib><creatorcontrib>Wen, Zhenzhen</creatorcontrib><creatorcontrib>Xu, Song</creatorcontrib><creatorcontrib>Shao, Wei</creatorcontrib><creatorcontrib>Cai, Jianting</creatorcontrib><creatorcontrib>Du, Qin</creatorcontrib><creatorcontrib>Zhu, Yongliang</creatorcontrib><creatorcontrib>Mao, Jianshan</creatorcontrib><title>Up-regulation of microRNA-1290 impairs cytokinesis and affects the reprogramming of colon cancer cells</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>► miR-1290 is up-regulated in colon cancer cells. ► Up-regulation of miR-1290 impairs cytokinesis. ► miR-1290 overexpression affects the reprogramming of colon cancer cells.
Abnormal cytokinesis increases the possibility of nuclear fusion in tumor cells. However, the role of microRNAs (miRNAs) in abnormal cytokinesis is unclear. Here, we found that miR-1290 was significantly up-regulated in clinical colon cancer tissues. Up-regulation of miR-1290 postponed cytokinesis and led to the formation of multinucleated cells. KIF13B was a target of miR-1290 that was involved in aberrant cytokinesis. Furthermore, enforced expression of miR-1290 activated the Wnt pathway and increased the reprogramming-related transcript factors c-Myc and Nanog. Our results suggest that up-regulation of miR-1290 in colon cancer cells impaired cytokinesis and affected reprogramming.</description><subject>Adenoma - genetics</subject><subject>Adenoma - metabolism</subject><subject>Adenoma - pathology</subject><subject>Base Sequence</subject><subject>Binding Sites</subject><subject>Breast cancer</subject><subject>Cell division</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Nucleus Division</subject><subject>Cell Proliferation</subject><subject>Chromosomes</subject><subject>Colon cancer</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colonic Neoplasms - pathology</subject><subject>Colorectal cancer</subject><subject>colorectal neoplasms</subject><subject>Cytokinesis</subject><subject>Cytokinesis - genetics</subject><subject>gene expression regulation</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Humans</subject><subject>Hybridization</subject><subject>KIF13B</subject><subject>Kinases</subject><subject>Kinesin - genetics</subject><subject>Kinesin - metabolism</subject><subject>microRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>MicroRNAs - physiology</subject><subject>miR-1290</subject><subject>Nanog Homeobox Protein</subject><subject>NF-kappa B - metabolism</subject><subject>Phosphatase</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><subject>RNA Interference</subject><subject>Studies</subject><subject>Transcription factors</subject><subject>Transcription, Genetic</subject><subject>Up-Regulation</subject><subject>Wnt Signaling Pathway</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk9rFTEUxYMo9rX6DUQH3HQzz5tkMkk2Qin-g6JgW3AXYubmmdeZyTOZEd63N8NUhW5cBS6_e3JyTgh5QWFLgbZv9ltnxx6nLQPKymgLXD0iG6okq6VW8JhsgENTc8XFCTnNeQ8AopHiKTlhnDaMabYh_vZQJ9zNvZ1CHKvoqyG4FL9-vqgp01CF4WBDypU7TvEujJhDruzYVdZ7dFOuph9YJTykuEt2GMK4WyRc7ItWsecwVQ77Pj8jT7ztMz6_P8_Izft3N5cf66svHz5dXlzVTnAx1V55Sa2WwBhK2radaDQHKQGdc15wq7yX0LhGKiaU4qApZVJrppzlouNn5HyVLYZ-zpgnM4S8GLAjxjmbAnMJJT5R0NcP0H2c01jMGdo2omRKdVuoZqVKJjkn9OaQwmDT0VAwSw1mb9YazFLDMi01lLWX9-Lz9wG7v0t_ci_AqxXwNhq7SyGb2-uiIEpHnDO53Px2JbDE9StgMtkFLIl2IZXkTRfD_zw8FHB9GIOz_R0eMf97rcnMgLlePsvyVygDaBv-jf8GTGe2eA</recordid><startdate>20130228</startdate><enddate>20130228</enddate><creator>Wu, Jia</creator><creator>Ji, Xiaowei</creator><creator>Zhu, Linlin</creator><creator>Jiang, Qiaoli</creator><creator>Wen, Zhenzhen</creator><creator>Xu, Song</creator><creator>Shao, Wei</creator><creator>Cai, Jianting</creator><creator>Du, Qin</creator><creator>Zhu, Yongliang</creator><creator>Mao, Jianshan</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Limited</general><scope>FBQ</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>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20130228</creationdate><title>Up-regulation of microRNA-1290 impairs cytokinesis and affects the reprogramming of colon cancer cells</title><author>Wu, Jia ; Ji, Xiaowei ; Zhu, Linlin ; Jiang, Qiaoli ; Wen, Zhenzhen ; Xu, Song ; Shao, Wei ; Cai, Jianting ; Du, Qin ; Zhu, Yongliang ; Mao, Jianshan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c535t-f8f71a97022e7166d54930770ecccf53a8ff704c478258830911279928ca35d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adenoma - genetics</topic><topic>Adenoma - metabolism</topic><topic>Adenoma - pathology</topic><topic>Base Sequence</topic><topic>Binding Sites</topic><topic>Breast cancer</topic><topic>Cell division</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Nucleus Division</topic><topic>Cell Proliferation</topic><topic>Chromosomes</topic><topic>Colon cancer</topic><topic>Colonic Neoplasms - genetics</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colonic Neoplasms - pathology</topic><topic>Colorectal cancer</topic><topic>colorectal neoplasms</topic><topic>Cytokinesis</topic><topic>Cytokinesis - genetics</topic><topic>gene expression regulation</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>Homeodomain Proteins - metabolism</topic><topic>Humans</topic><topic>Hybridization</topic><topic>KIF13B</topic><topic>Kinases</topic><topic>Kinesin - genetics</topic><topic>Kinesin - metabolism</topic><topic>microRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>MicroRNAs - physiology</topic><topic>miR-1290</topic><topic>Nanog Homeobox Protein</topic><topic>NF-kappa B - metabolism</topic><topic>Phosphatase</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Proto-Oncogene Proteins c-myc - metabolism</topic><topic>RNA Interference</topic><topic>Studies</topic><topic>Transcription factors</topic><topic>Transcription, Genetic</topic><topic>Up-Regulation</topic><topic>Wnt Signaling Pathway</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Jia</creatorcontrib><creatorcontrib>Ji, Xiaowei</creatorcontrib><creatorcontrib>Zhu, Linlin</creatorcontrib><creatorcontrib>Jiang, Qiaoli</creatorcontrib><creatorcontrib>Wen, Zhenzhen</creatorcontrib><creatorcontrib>Xu, Song</creatorcontrib><creatorcontrib>Shao, Wei</creatorcontrib><creatorcontrib>Cai, Jianting</creatorcontrib><creatorcontrib>Du, Qin</creatorcontrib><creatorcontrib>Zhu, Yongliang</creatorcontrib><creatorcontrib>Mao, Jianshan</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Jia</au><au>Ji, Xiaowei</au><au>Zhu, Linlin</au><au>Jiang, Qiaoli</au><au>Wen, Zhenzhen</au><au>Xu, Song</au><au>Shao, Wei</au><au>Cai, Jianting</au><au>Du, Qin</au><au>Zhu, Yongliang</au><au>Mao, Jianshan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Up-regulation of microRNA-1290 impairs cytokinesis and affects the reprogramming of colon cancer cells</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2013-02-28</date><risdate>2013</risdate><volume>329</volume><issue>2</issue><spage>155</spage><epage>163</epage><pages>155-163</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>► miR-1290 is up-regulated in colon cancer cells. ► Up-regulation of miR-1290 impairs cytokinesis. ► miR-1290 overexpression affects the reprogramming of colon cancer cells.
Abnormal cytokinesis increases the possibility of nuclear fusion in tumor cells. However, the role of microRNAs (miRNAs) in abnormal cytokinesis is unclear. Here, we found that miR-1290 was significantly up-regulated in clinical colon cancer tissues. Up-regulation of miR-1290 postponed cytokinesis and led to the formation of multinucleated cells. KIF13B was a target of miR-1290 that was involved in aberrant cytokinesis. Furthermore, enforced expression of miR-1290 activated the Wnt pathway and increased the reprogramming-related transcript factors c-Myc and Nanog. Our results suggest that up-regulation of miR-1290 in colon cancer cells impaired cytokinesis and affected reprogramming.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>23142292</pmid><doi>10.1016/j.canlet.2012.10.038</doi><tpages>9</tpages></addata></record> |
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subjects | Adenoma - genetics Adenoma - metabolism Adenoma - pathology Base Sequence Binding Sites Breast cancer Cell division Cell growth Cell Line, Tumor Cell Nucleus Division Cell Proliferation Chromosomes Colon cancer Colonic Neoplasms - genetics Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Colorectal cancer colorectal neoplasms Cytokinesis Cytokinesis - genetics gene expression regulation Gene Expression Regulation, Neoplastic Hematology, Oncology and Palliative Medicine Homeodomain Proteins - metabolism Humans Hybridization KIF13B Kinases Kinesin - genetics Kinesin - metabolism microRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism MicroRNAs - physiology miR-1290 Nanog Homeobox Protein NF-kappa B - metabolism Phosphatase Proteins Proto-Oncogene Proteins c-akt - metabolism Proto-Oncogene Proteins c-myc - metabolism RNA Interference Studies Transcription factors Transcription, Genetic Up-Regulation Wnt Signaling Pathway |
title | Up-regulation of microRNA-1290 impairs cytokinesis and affects the reprogramming of colon cancer cells |
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