LncRNA CASC15 promotes colon cancer cell proliferation and metastasis by regulating the miR‑4310/LGR5/Wnt/β‑catenin signaling pathway
Previous studies have indicated that overexpression of long noncoding RNA cancer susceptibility 15 (CASC15) may promote tumor development and progression in gastric cancer and hepatocellular carcinoma. However, the function of CASC15 in colon cancer remains unknown. In the present study, the express...
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Veröffentlicht in: | Molecular medicine reports 2018-08, Vol.18 (2), p.2269-2276 |
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description | Previous studies have indicated that overexpression of long noncoding RNA cancer susceptibility 15 (CASC15) may promote tumor development and progression in gastric cancer and hepatocellular carcinoma. However, the function of CASC15 in colon cancer remains unknown. In the present study, the expression of CASC15 was upregulated in colon cancer tissues and its expression was correlated with clinical Tumor‑Node‑Metastasis stage and tumor metastasis. In addition, knockdown of CASC15 significantly inhibited the proliferation, migration and invasion of colon cancer cells in vitro and in vivo. Following mechanistic experiments, CASC15 was observed to act as a sponge to suppress microRNA (miR)‑4310 that targeted LGR5. Through the inhibition of miR‑4310, CASC15 promoted leucine‑rich repeat‑containing G‑protein coupled receptor 5 (LGR5) expression and consequently activated the Wnt/β‑catenin signaling pathway. The results revealed that the inhibition of the Wnt/β‑catenin signaling pathway in CASC15‑overexpressing colon cancer cells suppressed cellular proliferation, migration and invasion. Collectively, these results demonstrated that CASC15 promoted colon cancer growth and metastasis through the activation of the Wnt/β‑catenin signaling pathway in a miR‑4310/LGR5 dependent manner. Thus, the present study suggested that CASC15 may be a therapeutic target for colon cancer treatment. |
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However, the function of CASC15 in colon cancer remains unknown. In the present study, the expression of CASC15 was upregulated in colon cancer tissues and its expression was correlated with clinical Tumor‑Node‑Metastasis stage and tumor metastasis. In addition, knockdown of CASC15 significantly inhibited the proliferation, migration and invasion of colon cancer cells in vitro and in vivo. Following mechanistic experiments, CASC15 was observed to act as a sponge to suppress microRNA (miR)‑4310 that targeted LGR5. Through the inhibition of miR‑4310, CASC15 promoted leucine‑rich repeat‑containing G‑protein coupled receptor 5 (LGR5) expression and consequently activated the Wnt/β‑catenin signaling pathway. The results revealed that the inhibition of the Wnt/β‑catenin signaling pathway in CASC15‑overexpressing colon cancer cells suppressed cellular proliferation, migration and invasion. Collectively, these results demonstrated that CASC15 promoted colon cancer growth and metastasis through the activation of the Wnt/β‑catenin signaling pathway in a miR‑4310/LGR5 dependent manner. Thus, the present study suggested that CASC15 may be a therapeutic target for colon cancer treatment.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2018.9191</identifier><identifier>PMID: 29956772</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>Apoptosis ; Cell growth ; Cell migration ; Cell proliferation ; Colon cancer ; Colorectal cancer ; G protein-coupled receptors ; Gastric cancer ; Hepatocellular carcinoma ; Hospitals ; Laboratory animals ; Leucine ; Liver cancer ; Lung cancer ; Medical prognosis ; Metastases ; Metastasis ; MicroRNAs ; miRNA ; Plasmids ; Proteins ; Regulation ; Signal transduction ; Studies ; Therapeutic applications ; Tumorigenesis ; Wnt protein ; β-Catenin</subject><ispartof>Molecular medicine reports, 2018-08, Vol.18 (2), p.2269-2276</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c290t-9bfd2849cf7d9a66a2768ef56b983d4a0b9a27bec9c1be9736a29205648655b93</citedby><cites>FETCH-LOGICAL-c290t-9bfd2849cf7d9a66a2768ef56b983d4a0b9a27bec9c1be9736a29205648655b93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29956772$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jing, Niancai</creatorcontrib><creatorcontrib>Huang, Tao</creatorcontrib><creatorcontrib>Guo, Huaiyu</creatorcontrib><creatorcontrib>Yang, Jili</creatorcontrib><creatorcontrib>Li, Mingjing</creatorcontrib><creatorcontrib>Chen, Zhuo</creatorcontrib><creatorcontrib>Zhang, Yue</creatorcontrib><title>LncRNA CASC15 promotes colon cancer cell proliferation and metastasis by regulating the miR‑4310/LGR5/Wnt/β‑catenin signaling pathway</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Previous studies have indicated that overexpression of long noncoding RNA cancer susceptibility 15 (CASC15) may promote tumor development and progression in gastric cancer and hepatocellular carcinoma. However, the function of CASC15 in colon cancer remains unknown. In the present study, the expression of CASC15 was upregulated in colon cancer tissues and its expression was correlated with clinical Tumor‑Node‑Metastasis stage and tumor metastasis. In addition, knockdown of CASC15 significantly inhibited the proliferation, migration and invasion of colon cancer cells in vitro and in vivo. Following mechanistic experiments, CASC15 was observed to act as a sponge to suppress microRNA (miR)‑4310 that targeted LGR5. Through the inhibition of miR‑4310, CASC15 promoted leucine‑rich repeat‑containing G‑protein coupled receptor 5 (LGR5) expression and consequently activated the Wnt/β‑catenin signaling pathway. The results revealed that the inhibition of the Wnt/β‑catenin signaling pathway in CASC15‑overexpressing colon cancer cells suppressed cellular proliferation, migration and invasion. Collectively, these results demonstrated that CASC15 promoted colon cancer growth and metastasis through the activation of the Wnt/β‑catenin signaling pathway in a miR‑4310/LGR5 dependent manner. Thus, the present study suggested that CASC15 may be a therapeutic target for colon cancer treatment.</description><subject>Apoptosis</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>G protein-coupled receptors</subject><subject>Gastric cancer</subject><subject>Hepatocellular carcinoma</subject><subject>Hospitals</subject><subject>Laboratory animals</subject><subject>Leucine</subject><subject>Liver cancer</subject><subject>Lung cancer</subject><subject>Medical prognosis</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Plasmids</subject><subject>Proteins</subject><subject>Regulation</subject><subject>Signal transduction</subject><subject>Studies</subject><subject>Therapeutic applications</subject><subject>Tumorigenesis</subject><subject>Wnt protein</subject><subject>β-Catenin</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkc1q3DAUhUVJ6CRpl90WQTbZeEY_luy7HIY0DQwNTFK6NLIsz3iw5YkkU2aXdXd9lT5IHiJPUpmZZBG4oMs5HwddDkJfKJnyHNis69yUEZpPgQL9gM5oBjThhKQnx50BZBN07v2WECmYgI9oEjUhs4ydoT9Lq1c_5ngxv19QgXeu7_pgPNZ921usldXGYW3adrTapjZOhSY6yla4M0H5OI3H5R47sx7aaNo1DhuDu2b18vQ35ZTMljcrMftlw-z5X5S0CsY2FvtmbVU74jsVNr_V_hM6rVXrzefje4F-frt-WHxPlnc3t4v5MtEMSEigrCuWp6DrrAIlpWKZzE0tZAk5r1JFSohSaTRoWhrIeCSAESHTXApRAr9AV4fceNHjYHwousaPJypr-sEXjEiW85xyEdHLd-i2H1z89kiBZILG-EglB0q73ntn6mLnmk65fUFJMZZUxJKKsaRiLCnyX4-pQ9mZ6o1-bYX_B6Wpj28</recordid><startdate>20180801</startdate><enddate>20180801</enddate><creator>Jing, Niancai</creator><creator>Huang, Tao</creator><creator>Guo, Huaiyu</creator><creator>Yang, Jili</creator><creator>Li, Mingjing</creator><creator>Chen, Zhuo</creator><creator>Zhang, Yue</creator><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20180801</creationdate><title>LncRNA CASC15 promotes colon cancer cell proliferation and metastasis by regulating the miR‑4310/LGR5/Wnt/β‑catenin signaling pathway</title><author>Jing, Niancai ; Huang, Tao ; Guo, Huaiyu ; Yang, Jili ; Li, Mingjing ; Chen, Zhuo ; Zhang, Yue</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c290t-9bfd2849cf7d9a66a2768ef56b983d4a0b9a27bec9c1be9736a29205648655b93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Apoptosis</topic><topic>Cell growth</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Colon cancer</topic><topic>Colorectal cancer</topic><topic>G protein-coupled receptors</topic><topic>Gastric cancer</topic><topic>Hepatocellular carcinoma</topic><topic>Hospitals</topic><topic>Laboratory animals</topic><topic>Leucine</topic><topic>Liver cancer</topic><topic>Lung cancer</topic><topic>Medical prognosis</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>Plasmids</topic><topic>Proteins</topic><topic>Regulation</topic><topic>Signal transduction</topic><topic>Studies</topic><topic>Therapeutic applications</topic><topic>Tumorigenesis</topic><topic>Wnt protein</topic><topic>β-Catenin</topic><toplevel>online_resources</toplevel><creatorcontrib>Jing, Niancai</creatorcontrib><creatorcontrib>Huang, Tao</creatorcontrib><creatorcontrib>Guo, Huaiyu</creatorcontrib><creatorcontrib>Yang, Jili</creatorcontrib><creatorcontrib>Li, Mingjing</creatorcontrib><creatorcontrib>Chen, Zhuo</creatorcontrib><creatorcontrib>Zhang, Yue</creatorcontrib><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>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science 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><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jing, Niancai</au><au>Huang, Tao</au><au>Guo, Huaiyu</au><au>Yang, Jili</au><au>Li, Mingjing</au><au>Chen, Zhuo</au><au>Zhang, Yue</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LncRNA CASC15 promotes colon cancer cell proliferation and metastasis by regulating the miR‑4310/LGR5/Wnt/β‑catenin signaling pathway</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-08-01</date><risdate>2018</risdate><volume>18</volume><issue>2</issue><spage>2269</spage><epage>2276</epage><pages>2269-2276</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Previous studies have indicated that overexpression of long noncoding RNA cancer susceptibility 15 (CASC15) may promote tumor development and progression in gastric cancer and hepatocellular carcinoma. However, the function of CASC15 in colon cancer remains unknown. In the present study, the expression of CASC15 was upregulated in colon cancer tissues and its expression was correlated with clinical Tumor‑Node‑Metastasis stage and tumor metastasis. In addition, knockdown of CASC15 significantly inhibited the proliferation, migration and invasion of colon cancer cells in vitro and in vivo. Following mechanistic experiments, CASC15 was observed to act as a sponge to suppress microRNA (miR)‑4310 that targeted LGR5. Through the inhibition of miR‑4310, CASC15 promoted leucine‑rich repeat‑containing G‑protein coupled receptor 5 (LGR5) expression and consequently activated the Wnt/β‑catenin signaling pathway. The results revealed that the inhibition of the Wnt/β‑catenin signaling pathway in CASC15‑overexpressing colon cancer cells suppressed cellular proliferation, migration and invasion. Collectively, these results demonstrated that CASC15 promoted colon cancer growth and metastasis through the activation of the Wnt/β‑catenin signaling pathway in a miR‑4310/LGR5 dependent manner. Thus, the present study suggested that CASC15 may be a therapeutic target for colon cancer treatment.</abstract><cop>Greece</cop><pub>Spandidos Publications UK Ltd</pub><pmid>29956772</pmid><doi>10.3892/mmr.2018.9191</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Apoptosis Cell growth Cell migration Cell proliferation Colon cancer Colorectal cancer G protein-coupled receptors Gastric cancer Hepatocellular carcinoma Hospitals Laboratory animals Leucine Liver cancer Lung cancer Medical prognosis Metastases Metastasis MicroRNAs miRNA Plasmids Proteins Regulation Signal transduction Studies Therapeutic applications Tumorigenesis Wnt protein β-Catenin |
title | LncRNA CASC15 promotes colon cancer cell proliferation and metastasis by regulating the miR‑4310/LGR5/Wnt/β‑catenin signaling pathway |
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