PVT1 Promotes the Proliferation and Migration of Non-Small Cell Lung Cancer via Regulating miR-148/RAB34 Signal Axis
It has been verified that long non-coding RNAs (lncRNAs) play critical roles in the development of human cancers. Increasing evidence indicates that lncRNA human plasmacytoma variant translocation1 (PVT1) was dysregulated in non-small cell lung cancer (NSCLC) which is the leading cause of cancer-rel...
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Veröffentlicht in: | OncoTargets and therapy 2020-02, Vol.13, p.1819-1832 |
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description | It has been verified that long non-coding RNAs (lncRNAs) play critical roles in the development of human cancers. Increasing evidence indicates that lncRNA human plasmacytoma variant translocation1 (PVT1) was dysregulated in non-small cell lung cancer (NSCLC) which is the leading cause of cancer-related death. However, the precise mechanism underlying the effect of PVT1 remains elusive. Our research focused on the correlation of PVT1 to miR-148 and RAB34 in NSCLC.
The quantitative real-time PCR (qRT-PCR) and western blot assay were used to detect gene and protein expression in NSCLC tissues and cells. CCK8, colony formation, transwell and wound healing assays were performed to evaluate the cell function of NSCLC cells. Dual-luciferase activity assay and RNA pull down assays were performed to verify the interaction between miR-148 and its targets. A xenograft test was conducted to detect the impact of RAB34 on tumor development in vitro.
In NSCLC tissues and cells, PVT1 and RAB34 were up-regulated, and miR-148 was down-regulated. Overexpression of PVT1 was capable of promoting NSCLC cell proliferation and migration which could be reversed by miR-148 restoration or RAB34 knock down. Also, our data firstly determined that the down-regulation of RAB34 had inhibitor effects while the up-regulation of RAB34 had promotive effects on tumor growth in vitro and in vivo.
Those findings indicated that the signal pathway PVT1/miR-148/RAB34 play critical roles in the progression of NSCLC could be proposed in NSCLC as a possible diagnosis or therapeutic targets. |
doi_str_mv | 10.2147/OTT.S222898 |
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The quantitative real-time PCR (qRT-PCR) and western blot assay were used to detect gene and protein expression in NSCLC tissues and cells. CCK8, colony formation, transwell and wound healing assays were performed to evaluate the cell function of NSCLC cells. Dual-luciferase activity assay and RNA pull down assays were performed to verify the interaction between miR-148 and its targets. A xenograft test was conducted to detect the impact of RAB34 on tumor development in vitro.
In NSCLC tissues and cells, PVT1 and RAB34 were up-regulated, and miR-148 was down-regulated. Overexpression of PVT1 was capable of promoting NSCLC cell proliferation and migration which could be reversed by miR-148 restoration or RAB34 knock down. Also, our data firstly determined that the down-regulation of RAB34 had inhibitor effects while the up-regulation of RAB34 had promotive effects on tumor growth in vitro and in vivo.
Those findings indicated that the signal pathway PVT1/miR-148/RAB34 play critical roles in the progression of NSCLC could be proposed in NSCLC as a possible diagnosis or therapeutic targets.</description><identifier>ISSN: 1178-6930</identifier><identifier>EISSN: 1178-6930</identifier><identifier>DOI: 10.2147/OTT.S222898</identifier><identifier>PMID: 32184617</identifier><language>eng</language><publisher>New Zealand: Dove Medical Press Limited</publisher><subject>Cholecystokinin ; Death ; Development and progression ; Genes ; Genetic research ; Health aspects ; Luciferase ; Lung cancer ; Lymphomas ; Non-small cell lung cancer ; Original Research ; Plasmacytoma ; RNA ; Small cell lung cancer ; Time ; Tumors ; Wound care ; Wound healing</subject><ispartof>OncoTargets and therapy, 2020-02, Vol.13, p.1819-1832</ispartof><rights>2020 Xi et al.</rights><rights>COPYRIGHT 2020 Dove Medical Press Limited</rights><rights>2020 Xi et al. 2020 Xi et al.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c521t-ecf2879ab34aa6c7f31b040247417453297f4f866cface7a8a1101d31b9894bc3</citedby><cites>FETCH-LOGICAL-c521t-ecf2879ab34aa6c7f31b040247417453297f4f866cface7a8a1101d31b9894bc3</cites><orcidid>0000-0003-2618-2052</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7054901/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7054901/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,3862,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32184617$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xi, Yong</creatorcontrib><creatorcontrib>Shen, Weiyu</creatorcontrib><creatorcontrib>Jin, Chenghua</creatorcontrib><creatorcontrib>Wang, Lijie</creatorcontrib><creatorcontrib>Yu, Bengtong</creatorcontrib><title>PVT1 Promotes the Proliferation and Migration of Non-Small Cell Lung Cancer via Regulating miR-148/RAB34 Signal Axis</title><title>OncoTargets and therapy</title><addtitle>Onco Targets Ther</addtitle><description>It has been verified that long non-coding RNAs (lncRNAs) play critical roles in the development of human cancers. Increasing evidence indicates that lncRNA human plasmacytoma variant translocation1 (PVT1) was dysregulated in non-small cell lung cancer (NSCLC) which is the leading cause of cancer-related death. However, the precise mechanism underlying the effect of PVT1 remains elusive. Our research focused on the correlation of PVT1 to miR-148 and RAB34 in NSCLC.
The quantitative real-time PCR (qRT-PCR) and western blot assay were used to detect gene and protein expression in NSCLC tissues and cells. CCK8, colony formation, transwell and wound healing assays were performed to evaluate the cell function of NSCLC cells. Dual-luciferase activity assay and RNA pull down assays were performed to verify the interaction between miR-148 and its targets. A xenograft test was conducted to detect the impact of RAB34 on tumor development in vitro.
In NSCLC tissues and cells, PVT1 and RAB34 were up-regulated, and miR-148 was down-regulated. Overexpression of PVT1 was capable of promoting NSCLC cell proliferation and migration which could be reversed by miR-148 restoration or RAB34 knock down. Also, our data firstly determined that the down-regulation of RAB34 had inhibitor effects while the up-regulation of RAB34 had promotive effects on tumor growth in vitro and in vivo.
Those findings indicated that the signal pathway PVT1/miR-148/RAB34 play critical roles in the progression of NSCLC could be proposed in NSCLC as a possible diagnosis or therapeutic targets.</description><subject>Cholecystokinin</subject><subject>Death</subject><subject>Development and progression</subject><subject>Genes</subject><subject>Genetic research</subject><subject>Health aspects</subject><subject>Luciferase</subject><subject>Lung cancer</subject><subject>Lymphomas</subject><subject>Non-small cell lung cancer</subject><subject>Original Research</subject><subject>Plasmacytoma</subject><subject>RNA</subject><subject>Small cell lung cancer</subject><subject>Time</subject><subject>Tumors</subject><subject>Wound care</subject><subject>Wound healing</subject><issn>1178-6930</issn><issn>1178-6930</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNptkl2LEzEUhgdxcT_0ynsJCCLIdPPVSeZmoRbXFaq7tNXbcJom00gmWSczy_rvN6V1aUECyTknz3nhJG9RvCV4RAkXl7fL5WhBKZW1fFGcESJkWdUMvzyIT4vzlH5jXFWS8lfFKaNE8oqIs6K_-7Uk6K6LbexNQv3GbBPvrOmgdzEgCGv03TX7LFr0I4Zy0YL3aGryNhtCg6YQtOnQgwM0N83gM5yrrZuXhMvL-eQz42jhmgAeTR5del2cWPDJvNmfF8XP6y_L6U05u_36bTqZlXpMSV8abakUNawYB6i0sIysMMeUC04EHzNaC8utrCptQRsBEgjBZJ2pWtZ8pdlFcbXTvR9WrVlrE_oOvLrvXAvdXxXBqeOb4DaqiQ9K4DGvMckCH_cCXfwzmNSr1iWdx4Zg4pAUZUJKkWmZ0fc7tAFvlAs2ZkW9xdWkIpLhTI0zNfoPldfatE7HYKzL9aOGDwcNGwO-36Toh-1vpGPw0w7UXUypM_Z5TILV1icq-0TtfZLpd4cv88z-MwZ7ApkUtWw</recordid><startdate>20200201</startdate><enddate>20200201</enddate><creator>Xi, Yong</creator><creator>Shen, Weiyu</creator><creator>Jin, Chenghua</creator><creator>Wang, Lijie</creator><creator>Yu, Bengtong</creator><general>Dove Medical Press Limited</general><general>Dove</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2618-2052</orcidid></search><sort><creationdate>20200201</creationdate><title>PVT1 Promotes the Proliferation and Migration of Non-Small Cell Lung Cancer via Regulating miR-148/RAB34 Signal Axis</title><author>Xi, Yong ; Shen, Weiyu ; Jin, Chenghua ; Wang, Lijie ; Yu, Bengtong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c521t-ecf2879ab34aa6c7f31b040247417453297f4f866cface7a8a1101d31b9894bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Cholecystokinin</topic><topic>Death</topic><topic>Development and progression</topic><topic>Genes</topic><topic>Genetic research</topic><topic>Health aspects</topic><topic>Luciferase</topic><topic>Lung cancer</topic><topic>Lymphomas</topic><topic>Non-small cell lung cancer</topic><topic>Original Research</topic><topic>Plasmacytoma</topic><topic>RNA</topic><topic>Small cell lung cancer</topic><topic>Time</topic><topic>Tumors</topic><topic>Wound care</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xi, Yong</creatorcontrib><creatorcontrib>Shen, Weiyu</creatorcontrib><creatorcontrib>Jin, Chenghua</creatorcontrib><creatorcontrib>Wang, Lijie</creatorcontrib><creatorcontrib>Yu, Bengtong</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>OncoTargets and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xi, Yong</au><au>Shen, Weiyu</au><au>Jin, Chenghua</au><au>Wang, Lijie</au><au>Yu, Bengtong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PVT1 Promotes the Proliferation and Migration of Non-Small Cell Lung Cancer via Regulating miR-148/RAB34 Signal Axis</atitle><jtitle>OncoTargets and therapy</jtitle><addtitle>Onco Targets Ther</addtitle><date>2020-02-01</date><risdate>2020</risdate><volume>13</volume><spage>1819</spage><epage>1832</epage><pages>1819-1832</pages><issn>1178-6930</issn><eissn>1178-6930</eissn><abstract>It has been verified that long non-coding RNAs (lncRNAs) play critical roles in the development of human cancers. Increasing evidence indicates that lncRNA human plasmacytoma variant translocation1 (PVT1) was dysregulated in non-small cell lung cancer (NSCLC) which is the leading cause of cancer-related death. However, the precise mechanism underlying the effect of PVT1 remains elusive. Our research focused on the correlation of PVT1 to miR-148 and RAB34 in NSCLC.
The quantitative real-time PCR (qRT-PCR) and western blot assay were used to detect gene and protein expression in NSCLC tissues and cells. CCK8, colony formation, transwell and wound healing assays were performed to evaluate the cell function of NSCLC cells. Dual-luciferase activity assay and RNA pull down assays were performed to verify the interaction between miR-148 and its targets. A xenograft test was conducted to detect the impact of RAB34 on tumor development in vitro.
In NSCLC tissues and cells, PVT1 and RAB34 were up-regulated, and miR-148 was down-regulated. Overexpression of PVT1 was capable of promoting NSCLC cell proliferation and migration which could be reversed by miR-148 restoration or RAB34 knock down. Also, our data firstly determined that the down-regulation of RAB34 had inhibitor effects while the up-regulation of RAB34 had promotive effects on tumor growth in vitro and in vivo.
Those findings indicated that the signal pathway PVT1/miR-148/RAB34 play critical roles in the progression of NSCLC could be proposed in NSCLC as a possible diagnosis or therapeutic targets.</abstract><cop>New Zealand</cop><pub>Dove Medical Press Limited</pub><pmid>32184617</pmid><doi>10.2147/OTT.S222898</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0003-2618-2052</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Cholecystokinin Death Development and progression Genes Genetic research Health aspects Luciferase Lung cancer Lymphomas Non-small cell lung cancer Original Research Plasmacytoma RNA Small cell lung cancer Time Tumors Wound care Wound healing |
title | PVT1 Promotes the Proliferation and Migration of Non-Small Cell Lung Cancer via Regulating miR-148/RAB34 Signal Axis |
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