Hsa-miR-326 targets CCND1 and inhibits non-small cell lung cancer development
Hsa-miRNA-326 (miR-326) has recently been discovered having anticancer efficacy in different organs. However, the role of miR-326 on non-small cell lung cancer (NSCLC) is still ambiguous. In this study, we investigated the role of miR-326 on the development of NSCLC. The results indicated that miR-3...
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| Veröffentlicht in: | Oncotarget 2016-02, Vol.7 (7), p.8341-8359 |
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| creator | Sun, Chengcao Huang, Chuanfeng Li, Shujun Yang, Cuili Xi, Yongyong Wang, Liang Zhang, Feng Fu, Yunfeng Li, Dejia |
| description | Hsa-miRNA-326 (miR-326) has recently been discovered having anticancer efficacy in different organs. However, the role of miR-326 on non-small cell lung cancer (NSCLC) is still ambiguous. In this study, we investigated the role of miR-326 on the development of NSCLC. The results indicated that miR-326 was significantly down-regulated in primary tumor tissues and very low levels were found in NSCLC cell lines. Ectopic expression of miR-326 in NSCLC cell lines significantly suppressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibition of cyclin D1, cyclin D2, CDK4 and up-regulation of p57(Kip2) and p21(Waf1/Cip1). In addition, miR-326 induced apoptosis, as indicated by concomitantly with up-regulation of key apoptosis protein cleaved caspase-3, and down-regulation of anti-apoptosis protein Bcl2. Moreover, miR-326 inhibited cellular migration and invasiveness through inhibition of matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene CCND1 was revealed to be a putative target of miR-326, which was inversely correlated with miR-326 expression in NSCLC. Taken together, our results demonstrated that miR-326 played a pivotal role on NSCLC through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic CCND1. |
| doi_str_mv | 10.18632/oncotarget.7071 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4884997</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1776629407</sourcerecordid><originalsourceid>FETCH-LOGICAL-c354t-502afecba21230a8826c810797b3b1ce971576ea1b3e2ee3c08a2bc09eb4a5a03</originalsourceid><addsrcrecordid>eNpVUUtPwkAQ3hiNEOTuyfTopbiPtrt7MTH4wAQ1MXreTJcBatpd7LYk_nuLIOIcZibz-ObxEXLO6IipTPAr76xvoF5gM5JUsiPSZzrRMU9TcXzg98gwhA_aSZpIxfUp6fFMJZQy1SdPkwBxVbzGgmfRFixE4_HzLYvAzaLCLYu86ELOuzhUUJaRxU6VrVtEFpzFOprhGku_qtA1Z-RkDmXA4c4OyPv93dt4Ek9fHh7HN9PYijRp4pRymKPNgTMuKCjFM6sYlVrmImcWtWSpzBBYLpAjCksV8NxSjXkCKVAxINdb3FWbVziz3egaSrOqiwrqL-OhMP8zrliahV-bRKlEa9kBXO4Aav_ZYmhMVYTNZeDQt8EwKbOM64RuSum21NY-hBrn-zGMmh8izB8RZkNE13JxuN6-4fft4hvz2Ybn</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1776629407</pqid></control><display><type>article</type><title>Hsa-miR-326 targets CCND1 and inhibits non-small cell lung cancer development</title><source>MEDLINE</source><source>PubMed Central Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free E- Journals</source><creator>Sun, Chengcao ; Huang, Chuanfeng ; Li, Shujun ; Yang, Cuili ; Xi, Yongyong ; Wang, Liang ; Zhang, Feng ; Fu, Yunfeng ; Li, Dejia</creator><creatorcontrib>Sun, Chengcao ; Huang, Chuanfeng ; Li, Shujun ; Yang, Cuili ; Xi, Yongyong ; Wang, Liang ; Zhang, Feng ; Fu, Yunfeng ; Li, Dejia</creatorcontrib><description>Hsa-miRNA-326 (miR-326) has recently been discovered having anticancer efficacy in different organs. However, the role of miR-326 on non-small cell lung cancer (NSCLC) is still ambiguous. In this study, we investigated the role of miR-326 on the development of NSCLC. The results indicated that miR-326 was significantly down-regulated in primary tumor tissues and very low levels were found in NSCLC cell lines. Ectopic expression of miR-326 in NSCLC cell lines significantly suppressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibition of cyclin D1, cyclin D2, CDK4 and up-regulation of p57(Kip2) and p21(Waf1/Cip1). In addition, miR-326 induced apoptosis, as indicated by concomitantly with up-regulation of key apoptosis protein cleaved caspase-3, and down-regulation of anti-apoptosis protein Bcl2. Moreover, miR-326 inhibited cellular migration and invasiveness through inhibition of matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene CCND1 was revealed to be a putative target of miR-326, which was inversely correlated with miR-326 expression in NSCLC. Taken together, our results demonstrated that miR-326 played a pivotal role on NSCLC through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic CCND1.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.7071</identifier><identifier>PMID: 26840018</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>Animals ; Apoptosis ; Blotting, Western ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell Movement ; Cell Proliferation ; Cyclin D1 - genetics ; Cyclin D1 - metabolism ; Fluorescent Antibody Technique ; Follow-Up Studies ; Gene Expression Regulation, Neoplastic ; Humans ; Immunoenzyme Techniques ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs - genetics ; Neoplasm Staging ; Prognosis ; Real-Time Polymerase Chain Reaction ; Research Paper ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; Survival Rate ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays</subject><ispartof>Oncotarget, 2016-02, Vol.7 (7), p.8341-8359</ispartof><rights>Copyright: © 2016 Sun et al. 2016</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c354t-502afecba21230a8826c810797b3b1ce971576ea1b3e2ee3c08a2bc09eb4a5a03</citedby><cites>FETCH-LOGICAL-c354t-502afecba21230a8826c810797b3b1ce971576ea1b3e2ee3c08a2bc09eb4a5a03</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/PMC4884997/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4884997/$$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/26840018$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Chengcao</creatorcontrib><creatorcontrib>Huang, Chuanfeng</creatorcontrib><creatorcontrib>Li, Shujun</creatorcontrib><creatorcontrib>Yang, Cuili</creatorcontrib><creatorcontrib>Xi, Yongyong</creatorcontrib><creatorcontrib>Wang, Liang</creatorcontrib><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Fu, Yunfeng</creatorcontrib><creatorcontrib>Li, Dejia</creatorcontrib><title>Hsa-miR-326 targets CCND1 and inhibits non-small cell lung cancer development</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>Hsa-miRNA-326 (miR-326) has recently been discovered having anticancer efficacy in different organs. However, the role of miR-326 on non-small cell lung cancer (NSCLC) is still ambiguous. In this study, we investigated the role of miR-326 on the development of NSCLC. The results indicated that miR-326 was significantly down-regulated in primary tumor tissues and very low levels were found in NSCLC cell lines. Ectopic expression of miR-326 in NSCLC cell lines significantly suppressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibition of cyclin D1, cyclin D2, CDK4 and up-regulation of p57(Kip2) and p21(Waf1/Cip1). In addition, miR-326 induced apoptosis, as indicated by concomitantly with up-regulation of key apoptosis protein cleaved caspase-3, and down-regulation of anti-apoptosis protein Bcl2. Moreover, miR-326 inhibited cellular migration and invasiveness through inhibition of matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene CCND1 was revealed to be a putative target of miR-326, which was inversely correlated with miR-326 expression in NSCLC. Taken together, our results demonstrated that miR-326 played a pivotal role on NSCLC through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic CCND1.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Blotting, Western</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cyclin D1 - genetics</subject><subject>Cyclin D1 - metabolism</subject><subject>Fluorescent Antibody Technique</subject><subject>Follow-Up Studies</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>MicroRNAs - genetics</subject><subject>Neoplasm Staging</subject><subject>Prognosis</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Research Paper</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Survival Rate</subject><subject>Tumor Cells, Cultured</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1949-2553</issn><issn>1949-2553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUUtPwkAQ3hiNEOTuyfTopbiPtrt7MTH4wAQ1MXreTJcBatpd7LYk_nuLIOIcZibz-ObxEXLO6IipTPAr76xvoF5gM5JUsiPSZzrRMU9TcXzg98gwhA_aSZpIxfUp6fFMJZQy1SdPkwBxVbzGgmfRFixE4_HzLYvAzaLCLYu86ELOuzhUUJaRxU6VrVtEFpzFOprhGku_qtA1Z-RkDmXA4c4OyPv93dt4Ek9fHh7HN9PYijRp4pRymKPNgTMuKCjFM6sYlVrmImcWtWSpzBBYLpAjCksV8NxSjXkCKVAxINdb3FWbVziz3egaSrOqiwrqL-OhMP8zrliahV-bRKlEa9kBXO4Aav_ZYmhMVYTNZeDQt8EwKbOM64RuSum21NY-hBrn-zGMmh8izB8RZkNE13JxuN6-4fft4hvz2Ybn</recordid><startdate>20160216</startdate><enddate>20160216</enddate><creator>Sun, Chengcao</creator><creator>Huang, Chuanfeng</creator><creator>Li, Shujun</creator><creator>Yang, Cuili</creator><creator>Xi, Yongyong</creator><creator>Wang, Liang</creator><creator>Zhang, Feng</creator><creator>Fu, Yunfeng</creator><creator>Li, Dejia</creator><general>Impact Journals LLC</general><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><scope>5PM</scope></search><sort><creationdate>20160216</creationdate><title>Hsa-miR-326 targets CCND1 and inhibits non-small cell lung cancer development</title><author>Sun, Chengcao ; Huang, Chuanfeng ; Li, Shujun ; Yang, Cuili ; Xi, Yongyong ; Wang, Liang ; Zhang, Feng ; Fu, Yunfeng ; Li, Dejia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c354t-502afecba21230a8826c810797b3b1ce971576ea1b3e2ee3c08a2bc09eb4a5a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Blotting, Western</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cyclin D1 - genetics</topic><topic>Cyclin D1 - metabolism</topic><topic>Fluorescent Antibody Technique</topic><topic>Follow-Up Studies</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>MicroRNAs - genetics</topic><topic>Neoplasm Staging</topic><topic>Prognosis</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Research Paper</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Survival Rate</topic><topic>Tumor Cells, Cultured</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>online_resources</toplevel><creatorcontrib>Sun, Chengcao</creatorcontrib><creatorcontrib>Huang, Chuanfeng</creatorcontrib><creatorcontrib>Li, Shujun</creatorcontrib><creatorcontrib>Yang, Cuili</creatorcontrib><creatorcontrib>Xi, Yongyong</creatorcontrib><creatorcontrib>Wang, Liang</creatorcontrib><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Fu, Yunfeng</creatorcontrib><creatorcontrib>Li, Dejia</creatorcontrib><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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncotarget</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Chengcao</au><au>Huang, Chuanfeng</au><au>Li, Shujun</au><au>Yang, Cuili</au><au>Xi, Yongyong</au><au>Wang, Liang</au><au>Zhang, Feng</au><au>Fu, Yunfeng</au><au>Li, Dejia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hsa-miR-326 targets CCND1 and inhibits non-small cell lung cancer development</atitle><jtitle>Oncotarget</jtitle><addtitle>Oncotarget</addtitle><date>2016-02-16</date><risdate>2016</risdate><volume>7</volume><issue>7</issue><spage>8341</spage><epage>8359</epage><pages>8341-8359</pages><issn>1949-2553</issn><eissn>1949-2553</eissn><abstract>Hsa-miRNA-326 (miR-326) has recently been discovered having anticancer efficacy in different organs. However, the role of miR-326 on non-small cell lung cancer (NSCLC) is still ambiguous. In this study, we investigated the role of miR-326 on the development of NSCLC. The results indicated that miR-326 was significantly down-regulated in primary tumor tissues and very low levels were found in NSCLC cell lines. Ectopic expression of miR-326 in NSCLC cell lines significantly suppressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibition of cyclin D1, cyclin D2, CDK4 and up-regulation of p57(Kip2) and p21(Waf1/Cip1). In addition, miR-326 induced apoptosis, as indicated by concomitantly with up-regulation of key apoptosis protein cleaved caspase-3, and down-regulation of anti-apoptosis protein Bcl2. Moreover, miR-326 inhibited cellular migration and invasiveness through inhibition of matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene CCND1 was revealed to be a putative target of miR-326, which was inversely correlated with miR-326 expression in NSCLC. Taken together, our results demonstrated that miR-326 played a pivotal role on NSCLC through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic CCND1.</abstract><cop>United States</cop><pub>Impact Journals LLC</pub><pmid>26840018</pmid><doi>10.18632/oncotarget.7071</doi><tpages>19</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis Blotting, Western Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Cell Movement Cell Proliferation Cyclin D1 - genetics Cyclin D1 - metabolism Fluorescent Antibody Technique Follow-Up Studies Gene Expression Regulation, Neoplastic Humans Immunoenzyme Techniques Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology Mice Mice, Inbred BALB C Mice, Nude MicroRNAs - genetics Neoplasm Staging Prognosis Real-Time Polymerase Chain Reaction Research Paper Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Survival Rate Tumor Cells, Cultured Xenograft Model Antitumor Assays |
| title | Hsa-miR-326 targets CCND1 and inhibits non-small cell lung cancer development |
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