miR-190b promotes colorectal cancer progression through targeting forkhead box protein P2
microRNA-190b (miR-190b) is abnormally expressed in multiple types of cancer, however, its role in colorectal cancer (CRC) is largely unknown. In the present study, it was demonstrated that miR-190b expression was upregulated in CRC cell lines compared with the normal epithelial colon cell line. Kno...
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Veröffentlicht in: | Experimental and therapeutic medicine 2020-01, Vol.19 (1), p.79-84 |
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description | microRNA-190b (miR-190b) is abnormally expressed in multiple types of cancer, however, its role in colorectal cancer (CRC) is largely unknown. In the present study, it was demonstrated that miR-190b expression was upregulated in CRC cell lines compared with the normal epithelial colon cell line. Knockdown of miR-190b decreased proliferation, colony formation and invasion, and increased apoptosis of CRC cells. Furthermore, forkhead box protein P2 (FOXP2) was predicted as a target of miR-190b and further validated by luciferase activity reporter assay and western blotting. Rescue experiments showed that knockdown of FOXP2 reversed the inhibitory effects of miR-190b inhibitor on the behavior of the CRC cell lines. Taken together, the present study demonstrated the oncogenic role of miR-190b in CRC through regulation of FOXP2 expression. |
doi_str_mv | 10.3892/etm.2019.8175 |
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In the present study, it was demonstrated that miR-190b expression was upregulated in CRC cell lines compared with the normal epithelial colon cell line. Knockdown of miR-190b decreased proliferation, colony formation and invasion, and increased apoptosis of CRC cells. Furthermore, forkhead box protein P2 (FOXP2) was predicted as a target of miR-190b and further validated by luciferase activity reporter assay and western blotting. Rescue experiments showed that knockdown of FOXP2 reversed the inhibitory effects of miR-190b inhibitor on the behavior of the CRC cell lines. Taken together, the present study demonstrated the oncogenic role of miR-190b in CRC through regulation of FOXP2 expression.</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2019.8175</identifier><identifier>PMID: 31853275</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Apoptosis ; Biotechnology ; Bone cancer ; Cell growth ; Colorectal cancer ; Comparative analysis ; Experiments ; Gastric cancer ; Gene expression ; Luciferase ; MicroRNA ; Proteins ; Scientific equipment industry ; Statistical analysis</subject><ispartof>Experimental and therapeutic medicine, 2020-01, Vol.19 (1), p.79-84</ispartof><rights>Copyright: © Zhao et al.</rights><rights>COPYRIGHT 2020 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2020</rights><rights>Copyright: © Zhao et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-effb65e18428f9bddf65df4f9e2d304e9bb30911ac1bffc90d81d7c291972c0b3</citedby><cites>FETCH-LOGICAL-c412t-effb65e18428f9bddf65df4f9e2d304e9bb30911ac1bffc90d81d7c291972c0b3</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/PMC6909528/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6909528/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31853275$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Qiang</creatorcontrib><creatorcontrib>Liu, Chengkui</creatorcontrib><creatorcontrib>Cui, Qing</creatorcontrib><creatorcontrib>Luan, Xuerong</creatorcontrib><creatorcontrib>Wang, Qingfeng</creatorcontrib><creatorcontrib>Zhou, Chengfu</creatorcontrib><title>miR-190b promotes colorectal cancer progression through targeting forkhead box protein P2</title><title>Experimental and therapeutic medicine</title><addtitle>Exp Ther Med</addtitle><description>microRNA-190b (miR-190b) is abnormally expressed in multiple types of cancer, however, its role in colorectal cancer (CRC) is largely unknown. In the present study, it was demonstrated that miR-190b expression was upregulated in CRC cell lines compared with the normal epithelial colon cell line. Knockdown of miR-190b decreased proliferation, colony formation and invasion, and increased apoptosis of CRC cells. Furthermore, forkhead box protein P2 (FOXP2) was predicted as a target of miR-190b and further validated by luciferase activity reporter assay and western blotting. Rescue experiments showed that knockdown of FOXP2 reversed the inhibitory effects of miR-190b inhibitor on the behavior of the CRC cell lines. Taken together, the present study demonstrated the oncogenic role of miR-190b in CRC through regulation of FOXP2 expression.</description><subject>Apoptosis</subject><subject>Biotechnology</subject><subject>Bone cancer</subject><subject>Cell growth</subject><subject>Colorectal cancer</subject><subject>Comparative analysis</subject><subject>Experiments</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Luciferase</subject><subject>MicroRNA</subject><subject>Proteins</subject><subject>Scientific equipment industry</subject><subject>Statistical analysis</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptks-L1TAQx4so7rLu0asUvHjpM5M0bXIRlmX9AQuK6MFTSNNJX9Y2eSap6H9vyj5XV0wOGTKf-YbJfKvqKZAdE5K-xLzsKAG5E9DzB9Up9JI2QIA_PMZECjipzlO6IWXxDoTgj6sTBoIz2vPT6sviPjYgyVAfYlhCxlSbMIeIJuu5NtobjFtqipiSC77O-xjWaV9nHSfMzk-1DfHrHvVYD-HHhmZ0vv5An1SPrJ4Tnh_Ps-rz66tPl2-b6_dv3l1eXDemBZobtHboOIJoqbByGEfb8dG2ViIdGWlRDgMjEkAbGKw1kowCxt5QCbKnhgzsrHp1q3tYhwVHgz5HPatDdIuOP1XQTt3PeLdXU_iuOkkkp6IIvDgKxPBtxZTV4pLBedYew5oUZVT0vJNdV9Dn_6A3YY2-tFcoVkbS9wL-UJOeUTlvQ3nXbKLqogPOOsbaTWv3H6rsERdngkfryv29gua2wMSQUkR71yMQtdlBFTuozQ5qs0Phn_39MXf07-GzX84SsJU</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Zhao, Qiang</creator><creator>Liu, Chengkui</creator><creator>Cui, Qing</creator><creator>Luan, Xuerong</creator><creator>Wang, Qingfeng</creator><creator>Zhou, Chengfu</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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In the present study, it was demonstrated that miR-190b expression was upregulated in CRC cell lines compared with the normal epithelial colon cell line. Knockdown of miR-190b decreased proliferation, colony formation and invasion, and increased apoptosis of CRC cells. Furthermore, forkhead box protein P2 (FOXP2) was predicted as a target of miR-190b and further validated by luciferase activity reporter assay and western blotting. Rescue experiments showed that knockdown of FOXP2 reversed the inhibitory effects of miR-190b inhibitor on the behavior of the CRC cell lines. Taken together, the present study demonstrated the oncogenic role of miR-190b in CRC through regulation of FOXP2 expression.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>31853275</pmid><doi>10.3892/etm.2019.8175</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Apoptosis Biotechnology Bone cancer Cell growth Colorectal cancer Comparative analysis Experiments Gastric cancer Gene expression Luciferase MicroRNA Proteins Scientific equipment industry Statistical analysis |
title | miR-190b promotes colorectal cancer progression through targeting forkhead box protein P2 |
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