miR‑146a‑5p targets TCSF and influences cell growth and apoptosis to repress NSCLC progression
Several studies have indicated that microRNAs (miRs) mediate multiple pathways associated with tumorigenesis and progression. Our preliminary study experimentally verified that miR‑146a‑5p has a role in the biological behavior of non‑small cell lung cancer (NSCLC) cells. To perform further investiga...
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description | Several studies have indicated that microRNAs (miRs) mediate multiple pathways associated with tumorigenesis and progression. Our preliminary study experimentally verified that miR‑146a‑5p has a role in the biological behavior of non‑small cell lung cancer (NSCLC) cells. To perform further investigation of miR‑146a‑5p, the present study evaluated miR‑146a‑5p by targeting its downstream gene tumor collagenase stimulatory factor (TCSF) to influence cell viability, proliferation and apoptosis in NSCLC. Online sequence prediction, a thorough search of the open source database The Cancer Genome Atlas (TCGA), immunohistochemistry (IHC) of TCSF in clinical lung cancer tissues, and a dual‑luciferase assay, as well as assays to test viability, proliferation and apoptosis in vitro, were conducted to explain the targeted regulation association between miR‑146a‑5p and TCSF in NSCLC. The miRanda and TargetScanHuman database revealed that TCSF and miR‑146a‑5p had target binding sites. A luciferase reporter assay demonstrated that miR‑146a‑5p and TCSF did have complementary sequences (P |
doi_str_mv | 10.3892/or.2019.7030 |
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Our preliminary study experimentally verified that miR‑146a‑5p has a role in the biological behavior of non‑small cell lung cancer (NSCLC) cells. To perform further investigation of miR‑146a‑5p, the present study evaluated miR‑146a‑5p by targeting its downstream gene tumor collagenase stimulatory factor (TCSF) to influence cell viability, proliferation and apoptosis in NSCLC. Online sequence prediction, a thorough search of the open source database The Cancer Genome Atlas (TCGA), immunohistochemistry (IHC) of TCSF in clinical lung cancer tissues, and a dual‑luciferase assay, as well as assays to test viability, proliferation and apoptosis in vitro, were conducted to explain the targeted regulation association between miR‑146a‑5p and TCSF in NSCLC. The miRanda and TargetScanHuman database revealed that TCSF and miR‑146a‑5p had target binding sites. A luciferase reporter assay demonstrated that miR‑146a‑5p and TCSF did have complementary sequences (P<0.05). From the TCGA database, TCSF was highly expressed in lung adenocarcinoma and lung squamous cell carcinoma tissues when compared with normal lung tissues (P<0.05). Furthermore, the protein level of TCSF in cancerous lung tissues was determined by IHC, and it was concluded that TCSF protein was also upregulated in NSCLC tissues (P<0.001). A significant difference was identified following in vitro experiments for the NSCLC cell line A549, which revealed that miR‑146a‑5p and TCSF regulated cell viability, proliferation and apoptosis. In conclusion, the present study verified the target action association between TCSF and miR‑146a‑5p with high throughput data analysis and experimental results in NSCLC.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2019.7030</identifier><identifier>PMID: 30816543</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>A549 Cells ; Adenocarcinoma ; Adult ; Aged ; Apoptosis ; Apoptosis - genetics ; Basigin - genetics ; Basigin - metabolism ; Bevacizumab ; Binding sites ; Cancer ; Cancer cells ; Cancer genetics ; Cancer therapies ; Carcinoma ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - pathology ; Care and treatment ; Cell growth ; Cell Proliferation - genetics ; Crizotinib ; Datasets as Topic ; Development and progression ; Disease ; Disease Progression ; Female ; Gene Expression Regulation, Neoplastic ; Genes ; Genomes ; Genomics ; Growth factors ; Health aspects ; Humans ; Identification and classification ; Immunohistochemistry ; Information management ; Kinases ; Luciferase ; Lung - pathology ; Lung cancer ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Male ; Mediation ; Metabolism ; Metastasis ; MicroRNA ; MicroRNAs ; MicroRNAs - metabolism ; Middle Aged ; Mutation ; Non-small cell lung cancer ; Ontology ; Pathology ; Pemetrexed ; Physiological aspects ; Proteins ; RNA, Small Interfering - metabolism ; Small cell lung cancer ; Squamous cell carcinoma ; Tumors</subject><ispartof>Oncology reports, 2019-04, Vol.41 (4), p.2226-2240</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><rights>Copyright: © Huang et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-d90016e06336211fe88eca0fd44cdb1103e6c77148ab9460d4a5ff811706ba623</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,777,781,882,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30816543$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Wen-Ting</creatorcontrib><creatorcontrib>He, Rong-Quan</creatorcontrib><creatorcontrib>Li, Xiao-Jiao</creatorcontrib><creatorcontrib>Ma, Jie</creatorcontrib><creatorcontrib>Peng, Zhi-Gang</creatorcontrib><creatorcontrib>Zhong, Jin-Cai</creatorcontrib><creatorcontrib>Hu, Xiao-Hua</creatorcontrib><creatorcontrib>Chen, Gang</creatorcontrib><title>miR‑146a‑5p targets TCSF and influences cell growth and apoptosis to repress NSCLC progression</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Several studies have indicated that microRNAs (miRs) mediate multiple pathways associated with tumorigenesis and progression. Our preliminary study experimentally verified that miR‑146a‑5p has a role in the biological behavior of non‑small cell lung cancer (NSCLC) cells. To perform further investigation of miR‑146a‑5p, the present study evaluated miR‑146a‑5p by targeting its downstream gene tumor collagenase stimulatory factor (TCSF) to influence cell viability, proliferation and apoptosis in NSCLC. Online sequence prediction, a thorough search of the open source database The Cancer Genome Atlas (TCGA), immunohistochemistry (IHC) of TCSF in clinical lung cancer tissues, and a dual‑luciferase assay, as well as assays to test viability, proliferation and apoptosis in vitro, were conducted to explain the targeted regulation association between miR‑146a‑5p and TCSF in NSCLC. The miRanda and TargetScanHuman database revealed that TCSF and miR‑146a‑5p had target binding sites. A luciferase reporter assay demonstrated that miR‑146a‑5p and TCSF did have complementary sequences (P<0.05). From the TCGA database, TCSF was highly expressed in lung adenocarcinoma and lung squamous cell carcinoma tissues when compared with normal lung tissues (P<0.05). Furthermore, the protein level of TCSF in cancerous lung tissues was determined by IHC, and it was concluded that TCSF protein was also upregulated in NSCLC tissues (P<0.001). A significant difference was identified following in vitro experiments for the NSCLC cell line A549, which revealed that miR‑146a‑5p and TCSF regulated cell viability, proliferation and apoptosis. In conclusion, the present study verified the target action association between TCSF and miR‑146a‑5p with high throughput data analysis and experimental results in NSCLC.</description><subject>A549 Cells</subject><subject>Adenocarcinoma</subject><subject>Adult</subject><subject>Aged</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Basigin - genetics</subject><subject>Basigin - metabolism</subject><subject>Bevacizumab</subject><subject>Binding sites</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cancer genetics</subject><subject>Cancer therapies</subject><subject>Carcinoma</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Care and treatment</subject><subject>Cell growth</subject><subject>Cell Proliferation - genetics</subject><subject>Crizotinib</subject><subject>Datasets as Topic</subject><subject>Development and progression</subject><subject>Disease</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Identification and classification</subject><subject>Immunohistochemistry</subject><subject>Information management</subject><subject>Kinases</subject><subject>Luciferase</subject><subject>Lung - pathology</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>Mediation</subject><subject>Metabolism</subject><subject>Metastasis</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Non-small cell lung cancer</subject><subject>Ontology</subject><subject>Pathology</subject><subject>Pemetrexed</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Small cell lung cancer</subject><subject>Squamous cell carcinoma</subject><subject>Tumors</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkkGL1TAQx4so7vr05lkCgniwz0yTpu1FWIqrwkPBXcFbSNNpX5a2qUmqePMr-BX9JKbuurwnksMkmd_M8P8zSfIY6JaVVfbSum1GodoWlNE7ySkUFaQZZ3A33mkGKWP555PkgfdXlGYFFdX95ITREkTO2WnSjObjrx8_gQsVQz6ToFyPwZPL-uKcqKklZuqGBSeNnmgcBtI7-y3s_6TUbOdgvfEkWOJwdug9eX9R72oyO9uvT2Onh8m9Tg0eH93ETfLp_PVl_TbdfXjzrj7bpToHGtK2ohQEUsGYyAA6LEvUinYt57ptAChDoYsCeKmaigvacpV3XQkQNTVKZGyTvLruOy_NiK3GKTg1yNmZUbnv0iojjzOT2cvefpWCQ5bHuZvk-U0DZ78s6IMcjV81qwnt4mUGZUFXa3lEn_6DXtnFTVFepKKQaHpxQPVqQBmNtHGuXpvKs7yoilzkbB27_Q8VT4uj0XbCzsT_o4JnBwV7VEPYezssIZrtj8EX16B21nuH3a0ZQOW6PNI6uS6PXJcn4k8ODbyF_24L-w3E0r5v</recordid><startdate>20190401</startdate><enddate>20190401</enddate><creator>Huang, Wen-Ting</creator><creator>He, Rong-Quan</creator><creator>Li, Xiao-Jiao</creator><creator>Ma, Jie</creator><creator>Peng, Zhi-Gang</creator><creator>Zhong, Jin-Cai</creator><creator>Hu, Xiao-Hua</creator><creator>Chen, Gang</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190401</creationdate><title>miR‑146a‑5p targets TCSF and influences cell growth and apoptosis to repress NSCLC progression</title><author>Huang, Wen-Ting ; He, Rong-Quan ; Li, Xiao-Jiao ; Ma, Jie ; Peng, Zhi-Gang ; Zhong, Jin-Cai ; Hu, Xiao-Hua ; Chen, Gang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c510t-d90016e06336211fe88eca0fd44cdb1103e6c77148ab9460d4a5ff811706ba623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>A549 Cells</topic><topic>Adenocarcinoma</topic><topic>Adult</topic><topic>Aged</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Basigin - genetics</topic><topic>Basigin - metabolism</topic><topic>Bevacizumab</topic><topic>Binding sites</topic><topic>Cancer</topic><topic>Cancer cells</topic><topic>Cancer genetics</topic><topic>Cancer therapies</topic><topic>Carcinoma</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Care and treatment</topic><topic>Cell growth</topic><topic>Cell Proliferation - genetics</topic><topic>Crizotinib</topic><topic>Datasets as Topic</topic><topic>Development and progression</topic><topic>Disease</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Genomes</topic><topic>Genomics</topic><topic>Growth factors</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Identification and classification</topic><topic>Immunohistochemistry</topic><topic>Information management</topic><topic>Kinases</topic><topic>Luciferase</topic><topic>Lung - pathology</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>Mediation</topic><topic>Metabolism</topic><topic>Metastasis</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Non-small cell lung cancer</topic><topic>Ontology</topic><topic>Pathology</topic><topic>Pemetrexed</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Small cell lung cancer</topic><topic>Squamous cell carcinoma</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>Huang, Wen-Ting</creatorcontrib><creatorcontrib>He, Rong-Quan</creatorcontrib><creatorcontrib>Li, Xiao-Jiao</creatorcontrib><creatorcontrib>Ma, Jie</creatorcontrib><creatorcontrib>Peng, Zhi-Gang</creatorcontrib><creatorcontrib>Zhong, Jin-Cai</creatorcontrib><creatorcontrib>Hu, Xiao-Hua</creatorcontrib><creatorcontrib>Chen, Gang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Wen-Ting</au><au>He, Rong-Quan</au><au>Li, Xiao-Jiao</au><au>Ma, Jie</au><au>Peng, Zhi-Gang</au><au>Zhong, Jin-Cai</au><au>Hu, Xiao-Hua</au><au>Chen, Gang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR‑146a‑5p targets TCSF and influences cell growth and apoptosis to repress NSCLC progression</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2019-04-01</date><risdate>2019</risdate><volume>41</volume><issue>4</issue><spage>2226</spage><epage>2240</epage><pages>2226-2240</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Several studies have indicated that microRNAs (miRs) mediate multiple pathways associated with tumorigenesis and progression. Our preliminary study experimentally verified that miR‑146a‑5p has a role in the biological behavior of non‑small cell lung cancer (NSCLC) cells. To perform further investigation of miR‑146a‑5p, the present study evaluated miR‑146a‑5p by targeting its downstream gene tumor collagenase stimulatory factor (TCSF) to influence cell viability, proliferation and apoptosis in NSCLC. Online sequence prediction, a thorough search of the open source database The Cancer Genome Atlas (TCGA), immunohistochemistry (IHC) of TCSF in clinical lung cancer tissues, and a dual‑luciferase assay, as well as assays to test viability, proliferation and apoptosis in vitro, were conducted to explain the targeted regulation association between miR‑146a‑5p and TCSF in NSCLC. The miRanda and TargetScanHuman database revealed that TCSF and miR‑146a‑5p had target binding sites. A luciferase reporter assay demonstrated that miR‑146a‑5p and TCSF did have complementary sequences (P<0.05). From the TCGA database, TCSF was highly expressed in lung adenocarcinoma and lung squamous cell carcinoma tissues when compared with normal lung tissues (P<0.05). Furthermore, the protein level of TCSF in cancerous lung tissues was determined by IHC, and it was concluded that TCSF protein was also upregulated in NSCLC tissues (P<0.001). A significant difference was identified following in vitro experiments for the NSCLC cell line A549, which revealed that miR‑146a‑5p and TCSF regulated cell viability, proliferation and apoptosis. In conclusion, the present study verified the target action association between TCSF and miR‑146a‑5p with high throughput data analysis and experimental results in NSCLC.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30816543</pmid><doi>10.3892/or.2019.7030</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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subjects | A549 Cells Adenocarcinoma Adult Aged Apoptosis Apoptosis - genetics Basigin - genetics Basigin - metabolism Bevacizumab Binding sites Cancer Cancer cells Cancer genetics Cancer therapies Carcinoma Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - pathology Care and treatment Cell growth Cell Proliferation - genetics Crizotinib Datasets as Topic Development and progression Disease Disease Progression Female Gene Expression Regulation, Neoplastic Genes Genomes Genomics Growth factors Health aspects Humans Identification and classification Immunohistochemistry Information management Kinases Luciferase Lung - pathology Lung cancer Lung Neoplasms - genetics Lung Neoplasms - pathology Male Mediation Metabolism Metastasis MicroRNA MicroRNAs MicroRNAs - metabolism Middle Aged Mutation Non-small cell lung cancer Ontology Pathology Pemetrexed Physiological aspects Proteins RNA, Small Interfering - metabolism Small cell lung cancer Squamous cell carcinoma Tumors |
title | miR‑146a‑5p targets TCSF and influences cell growth and apoptosis to repress NSCLC progression |
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