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circRNA RNF111 regulates the growth, migration and invasion of gastric cancer cells by binding to miR‑27b‑3p
hsa_circ_0001982 [circRNA ring finger protein 111 (RNF111)] has been found to promote cancer growth; however, its role in gastric cancer (GC) remains unclear. The present study examined the effects of circR-RNF111 on the growth, migration and invasion of GC cells and aimed to elucidate the underlyin...
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Published in: | International journal of molecular medicine 2020-11, Vol.46 (5), p.1873-1885 |
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description | hsa_circ_0001982 [circRNA ring finger protein 111 (RNF111)] has been found to promote cancer growth; however, its role in gastric cancer (GC) remains unclear. The present study examined the effects of circR-RNF111 on the growth, migration and invasion of GC cells and aimed to elucidate the underlying molecular mechanisms. The expression levels of circR-RNF111 and miR-27b-3p in GC tissues and GC cell lines were detected by reverse transcription-quantitative PCR (RT-qPCR). StarBase v2.0 and dual-luciferase assay were used to predict and analyze the association between circR-RNF111 and miR-27b-3p. The effects of circR-RNF111 and miR-27b-3p on cell growth, apoptosis, migration and invasion were detected by cell counting kit-8 (CCK-8) assay, colony formation assay, flow cytometry, wound-healing assay and Transwell assay, respectively. In addition, western blot analysis was performed to determine the expression levels of genes related to cell apoptosis and epithelial-mesenchymal transition (EMT). The results revealed that circR-RNF111 and miR-27b-3p were closely related to the clinicopathological characteristics of GC, and that circR-RNF111 and miR-27b-3p negatively correlated and were abnormally expressed in GC. circR-RNF111 acted as a sponge of miR-27b-3p. The silencing of circR-RNF111 significantly inhibited GC cell viability, colony formation, migration and invasion, and exerted a pro-apoptotic effect. miR-27b-3p inhibitor promoted the proliferation, migration and invasion of GC cells, and inhibited cell apoptosis. In addition, circR-RNF111 silencing significantly decreased the expression levels of Bc12, Vimentin and N-cadherin, and increased those of cleaved caspase-3 and E-cadherin Furthermore, miR-27b-3p inhibition reversed the regulatory effects of circR-RNF111 silencing on the GC cells. On the whole, the findings of the present study demonstrate that circR-RNF111 is involved in the regulation of growth, migration and invasion of GC cells by binding to miR-27b-3p. |
doi_str_mv | 10.3892/ijmm.2020.4709 |
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The present study examined the effects of circR-RNF111 on the growth, migration and invasion of GC cells and aimed to elucidate the underlying molecular mechanisms. The expression levels of circR-RNF111 and miR-27b-3p in GC tissues and GC cell lines were detected by reverse transcription-quantitative PCR (RT-qPCR). StarBase v2.0 and dual-luciferase assay were used to predict and analyze the association between circR-RNF111 and miR-27b-3p. The effects of circR-RNF111 and miR-27b-3p on cell growth, apoptosis, migration and invasion were detected by cell counting kit-8 (CCK-8) assay, colony formation assay, flow cytometry, wound-healing assay and Transwell assay, respectively. In addition, western blot analysis was performed to determine the expression levels of genes related to cell apoptosis and epithelial-mesenchymal transition (EMT). The results revealed that circR-RNF111 and miR-27b-3p were closely related to the clinicopathological characteristics of GC, and that circR-RNF111 and miR-27b-3p negatively correlated and were abnormally expressed in GC. circR-RNF111 acted as a sponge of miR-27b-3p. The silencing of circR-RNF111 significantly inhibited GC cell viability, colony formation, migration and invasion, and exerted a pro-apoptotic effect. miR-27b-3p inhibitor promoted the proliferation, migration and invasion of GC cells, and inhibited cell apoptosis. In addition, circR-RNF111 silencing significantly decreased the expression levels of Bc12, Vimentin and N-cadherin, and increased those of cleaved caspase-3 and E-cadherin Furthermore, miR-27b-3p inhibition reversed the regulatory effects of circR-RNF111 silencing on the GC cells. On the whole, the findings of the present study demonstrate that circR-RNF111 is involved in the regulation of growth, migration and invasion of GC cells by binding to miR-27b-3p.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2020.4709</identifier><identifier>PMID: 33000178</identifier><language>eng</language><publisher>Athens: Spandidos Publications</publisher><subject>Analysis ; Apoptosis ; Binding sites ; Biomarkers ; Biotechnology ; Bladder cancer ; Cancer ; Cancer research ; Cloning ; Gastric cancer ; Genes ; Growth ; Luciferase ; Metastasis ; MicroRNAs ; Reagents ; Scientific equipment industry ; Stomach cancer</subject><ispartof>International journal of molecular medicine, 2020-11, Vol.46 (5), p.1873-1885</ispartof><rights>COPYRIGHT 2020 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2020</rights><rights>Copyright: © Wang et al. 2020</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c462t-1b4d956d9965b9d3302c557b028caefc76ac35335b77f3f2f826bf8fdd38fc663</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids></links><search><creatorcontrib>Wang, Zhibing</creatorcontrib><creatorcontrib>Jiang, Zongdan</creatorcontrib><creatorcontrib>Zhou, Jin</creatorcontrib><creatorcontrib>Liu, Zheng</creatorcontrib><title>circRNA RNF111 regulates the growth, migration and invasion of gastric cancer cells by binding to miR‑27b‑3p</title><title>International journal of molecular medicine</title><description>hsa_circ_0001982 [circRNA ring finger protein 111 (RNF111)] has been found to promote cancer growth; however, its role in gastric cancer (GC) remains unclear. The present study examined the effects of circR-RNF111 on the growth, migration and invasion of GC cells and aimed to elucidate the underlying molecular mechanisms. The expression levels of circR-RNF111 and miR-27b-3p in GC tissues and GC cell lines were detected by reverse transcription-quantitative PCR (RT-qPCR). StarBase v2.0 and dual-luciferase assay were used to predict and analyze the association between circR-RNF111 and miR-27b-3p. The effects of circR-RNF111 and miR-27b-3p on cell growth, apoptosis, migration and invasion were detected by cell counting kit-8 (CCK-8) assay, colony formation assay, flow cytometry, wound-healing assay and Transwell assay, respectively. In addition, western blot analysis was performed to determine the expression levels of genes related to cell apoptosis and epithelial-mesenchymal transition (EMT). The results revealed that circR-RNF111 and miR-27b-3p were closely related to the clinicopathological characteristics of GC, and that circR-RNF111 and miR-27b-3p negatively correlated and were abnormally expressed in GC. circR-RNF111 acted as a sponge of miR-27b-3p. The silencing of circR-RNF111 significantly inhibited GC cell viability, colony formation, migration and invasion, and exerted a pro-apoptotic effect. miR-27b-3p inhibitor promoted the proliferation, migration and invasion of GC cells, and inhibited cell apoptosis. In addition, circR-RNF111 silencing significantly decreased the expression levels of Bc12, Vimentin and N-cadherin, and increased those of cleaved caspase-3 and E-cadherin Furthermore, miR-27b-3p inhibition reversed the regulatory effects of circR-RNF111 silencing on the GC cells. On the whole, the findings of the present study demonstrate that circR-RNF111 is involved in the regulation of growth, migration and invasion of GC cells by binding to miR-27b-3p.</description><subject>Analysis</subject><subject>Apoptosis</subject><subject>Binding sites</subject><subject>Biomarkers</subject><subject>Biotechnology</subject><subject>Bladder cancer</subject><subject>Cancer</subject><subject>Cancer research</subject><subject>Cloning</subject><subject>Gastric cancer</subject><subject>Genes</subject><subject>Growth</subject><subject>Luciferase</subject><subject>Metastasis</subject><subject>MicroRNAs</subject><subject>Reagents</subject><subject>Scientific equipment industry</subject><subject>Stomach cancer</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNptUU2LFDEQbURx19Wr54BXe8xHJ-lchGFxVVhWGBS8hXz2ZOhOxiSzsjf_gn_RX2IaF0VYilQlqVePR72ue4nghowCvwmHZdlgiOFm4FA86s4RF6jHw_D1cbsjyHvCKTvrnpVygBDTQYxPuzNCIISIj-fd0YRsdjdbsLu5QgiB7KbTrKoroO4dmHL6XvevwRKmrGpIEahoQYi3qqyP5MGkSs3BAKOicRkYN88F6DugQ7QhTqCmNrz79eMn5rplcnzePfFqLu7Ffb3ovly9-3z5ob_-9P7j5fa6NwPDtUd6sIIyKwSjWtgmGBtKuYZ4NMp5w5kyhBJCNeeeeOxHzLQfvbVk9IYxctG9_cN7POnFWeNizWqWxxwWle9kUkH-34lhL6d0KznFiDLYCF7dE-T07eRKlYd0yrFplm2943oE_4ea1OxkiD41MrOEYuSWEdFWjtjQUJsHUC2sW4JJ0fnQ_h8aMDmVkp3_KxxBuRovV-PlarxcjSe_AVaeoMY</recordid><startdate>20201101</startdate><enddate>20201101</enddate><creator>Wang, Zhibing</creator><creator>Jiang, Zongdan</creator><creator>Zhou, Jin</creator><creator>Liu, Zheng</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20201101</creationdate><title>circRNA RNF111 regulates the growth, migration and invasion of gastric cancer cells by binding to miR‑27b‑3p</title><author>Wang, Zhibing ; Jiang, Zongdan ; Zhou, Jin ; Liu, Zheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c462t-1b4d956d9965b9d3302c557b028caefc76ac35335b77f3f2f826bf8fdd38fc663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Analysis</topic><topic>Apoptosis</topic><topic>Binding sites</topic><topic>Biomarkers</topic><topic>Biotechnology</topic><topic>Bladder cancer</topic><topic>Cancer</topic><topic>Cancer research</topic><topic>Cloning</topic><topic>Gastric cancer</topic><topic>Genes</topic><topic>Growth</topic><topic>Luciferase</topic><topic>Metastasis</topic><topic>MicroRNAs</topic><topic>Reagents</topic><topic>Scientific equipment industry</topic><topic>Stomach cancer</topic><toplevel>online_resources</toplevel><creatorcontrib>Wang, Zhibing</creatorcontrib><creatorcontrib>Jiang, Zongdan</creatorcontrib><creatorcontrib>Zhou, Jin</creatorcontrib><creatorcontrib>Liu, Zheng</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Proquest Health & Medical Complete</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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 China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Zhibing</au><au>Jiang, Zongdan</au><au>Zhou, Jin</au><au>Liu, Zheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>circRNA RNF111 regulates the growth, migration and invasion of gastric cancer cells by binding to miR‑27b‑3p</atitle><jtitle>International journal of molecular medicine</jtitle><date>2020-11-01</date><risdate>2020</risdate><volume>46</volume><issue>5</issue><spage>1873</spage><epage>1885</epage><pages>1873-1885</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>hsa_circ_0001982 [circRNA ring finger protein 111 (RNF111)] has been found to promote cancer growth; however, its role in gastric cancer (GC) remains unclear. The present study examined the effects of circR-RNF111 on the growth, migration and invasion of GC cells and aimed to elucidate the underlying molecular mechanisms. The expression levels of circR-RNF111 and miR-27b-3p in GC tissues and GC cell lines were detected by reverse transcription-quantitative PCR (RT-qPCR). StarBase v2.0 and dual-luciferase assay were used to predict and analyze the association between circR-RNF111 and miR-27b-3p. The effects of circR-RNF111 and miR-27b-3p on cell growth, apoptosis, migration and invasion were detected by cell counting kit-8 (CCK-8) assay, colony formation assay, flow cytometry, wound-healing assay and Transwell assay, respectively. In addition, western blot analysis was performed to determine the expression levels of genes related to cell apoptosis and epithelial-mesenchymal transition (EMT). The results revealed that circR-RNF111 and miR-27b-3p were closely related to the clinicopathological characteristics of GC, and that circR-RNF111 and miR-27b-3p negatively correlated and were abnormally expressed in GC. circR-RNF111 acted as a sponge of miR-27b-3p. The silencing of circR-RNF111 significantly inhibited GC cell viability, colony formation, migration and invasion, and exerted a pro-apoptotic effect. miR-27b-3p inhibitor promoted the proliferation, migration and invasion of GC cells, and inhibited cell apoptosis. In addition, circR-RNF111 silencing significantly decreased the expression levels of Bc12, Vimentin and N-cadherin, and increased those of cleaved caspase-3 and E-cadherin Furthermore, miR-27b-3p inhibition reversed the regulatory effects of circR-RNF111 silencing on the GC cells. On the whole, the findings of the present study demonstrate that circR-RNF111 is involved in the regulation of growth, migration and invasion of GC cells by binding to miR-27b-3p.</abstract><cop>Athens</cop><pub>Spandidos Publications</pub><pmid>33000178</pmid><doi>10.3892/ijmm.2020.4709</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Analysis Apoptosis Binding sites Biomarkers Biotechnology Bladder cancer Cancer Cancer research Cloning Gastric cancer Genes Growth Luciferase Metastasis MicroRNAs Reagents Scientific equipment industry Stomach cancer |
title | circRNA RNF111 regulates the growth, migration and invasion of gastric cancer cells by binding to miR‑27b‑3p |
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