C2orf48 promotes the progression of nasopharyngeal carcinoma by regulating high mobility group AT-hook 2
Recurrence and metastasis are the major factors affecting the survival of nasopharyngeal carcinoma (NPC), and the mechanism remains unclear. Long non-coding RNA chromosome 2 open reading frame 48 (C2orf48) has been shown to influence the prognosis of many cancers. However, C2orf48’s function in NPC...
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Veröffentlicht in: | Medical oncology (Northwood, London, England) London, England), 2023-09, Vol.40 (11), p.306-306, Article 306 |
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description | Recurrence and metastasis are the major factors affecting the survival of nasopharyngeal carcinoma (NPC), and the mechanism remains unclear. Long non-coding RNA chromosome 2 open reading frame 48 (C2orf48) has been shown to influence the prognosis of many cancers. However, C2orf48’s function in NPC has not been clarified. In this investigation, C2orf48 expression in NPC was measured by quantitative real-time PCR (qRT-PCR) at the cellular and tissue levels, and the association between C2orf48 expression and the prognosis of patients with NPC was examined. Additionally, the effects of C2orf48 and high mobility group AT-hook 2 (HMGA2) upon NPC proliferation, migration, and invasion were examined employing the MTT assay, colony formation assay, and transwell assay, respectively. Furthermore, the association between C2orf48 and HMGA2 in NPC was investigated. Our research demonstrated that C2orf48 was overexpressed in NPC tissues and cell lines, and compared to patients with lower levels of C2orf48 expression, those with higher levels had poorer 5-year overall survival and progression-free survival. Functionally, C2orf48 overexpression accelerated NPC cells proliferation, migration, and invasion. Besides, the tandem mass tag (TMT) quantitative proteomic analysis indicated that HMGA2 may be a target of C2orf48. Moreover, upregulation of C2orf48 could increase HMGA2 expression, and HMGA2 silencing could counteract the proliferation, migration, and invasion changes induced by C2orf48 in NPC cells. These results reveal that overexpression of C2orf48 can promote NPC cells proliferation, migration, and invasion via regulating the expression of HMGA2 and C2orf48 may be a potentially important prognostic marker for NPC. |
doi_str_mv | 10.1007/s12032-023-02179-3 |
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Long non-coding RNA chromosome 2 open reading frame 48 (C2orf48) has been shown to influence the prognosis of many cancers. However, C2orf48’s function in NPC has not been clarified. In this investigation, C2orf48 expression in NPC was measured by quantitative real-time PCR (qRT-PCR) at the cellular and tissue levels, and the association between C2orf48 expression and the prognosis of patients with NPC was examined. Additionally, the effects of C2orf48 and high mobility group AT-hook 2 (HMGA2) upon NPC proliferation, migration, and invasion were examined employing the MTT assay, colony formation assay, and transwell assay, respectively. Furthermore, the association between C2orf48 and HMGA2 in NPC was investigated. Our research demonstrated that C2orf48 was overexpressed in NPC tissues and cell lines, and compared to patients with lower levels of C2orf48 expression, those with higher levels had poorer 5-year overall survival and progression-free survival. Functionally, C2orf48 overexpression accelerated NPC cells proliferation, migration, and invasion. Besides, the tandem mass tag (TMT) quantitative proteomic analysis indicated that HMGA2 may be a target of C2orf48. Moreover, upregulation of C2orf48 could increase HMGA2 expression, and HMGA2 silencing could counteract the proliferation, migration, and invasion changes induced by C2orf48 in NPC cells. These results reveal that overexpression of C2orf48 can promote NPC cells proliferation, migration, and invasion via regulating the expression of HMGA2 and C2orf48 may be a potentially important prognostic marker for NPC.</description><identifier>ISSN: 1559-131X</identifier><identifier>ISSN: 1357-0560</identifier><identifier>EISSN: 1559-131X</identifier><identifier>DOI: 10.1007/s12032-023-02179-3</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Hematology ; Internal Medicine ; Medical prognosis ; Medicine ; Medicine & Public Health ; Oncology ; Original Paper ; Pathology ; Throat cancer</subject><ispartof>Medical oncology (Northwood, London, England), 2023-09, Vol.40 (11), p.306-306, Article 306</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c303t-ba1ee4ce93602c0e5bc3dbf2632d9792cd685189b3df3e621d83e672bf5840c83</cites><orcidid>0000-0002-5859-533X ; 0000-0001-6097-7794</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12032-023-02179-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12032-023-02179-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids></links><search><creatorcontrib>Jiang, Yanhui</creatorcontrib><creatorcontrib>Liang, Faya</creatorcontrib><creatorcontrib>Chen, Renhui</creatorcontrib><creatorcontrib>Huang, Yongsheng</creatorcontrib><creatorcontrib>Xiao, Zhiwen</creatorcontrib><creatorcontrib>Zeng, Haicang</creatorcontrib><creatorcontrib>Han, Ping</creatorcontrib><creatorcontrib>Huang, Xiaoming</creatorcontrib><title>C2orf48 promotes the progression of nasopharyngeal carcinoma by regulating high mobility group AT-hook 2</title><title>Medical oncology (Northwood, London, England)</title><addtitle>Med Oncol</addtitle><description>Recurrence and metastasis are the major factors affecting the survival of nasopharyngeal carcinoma (NPC), and the mechanism remains unclear. Long non-coding RNA chromosome 2 open reading frame 48 (C2orf48) has been shown to influence the prognosis of many cancers. However, C2orf48’s function in NPC has not been clarified. In this investigation, C2orf48 expression in NPC was measured by quantitative real-time PCR (qRT-PCR) at the cellular and tissue levels, and the association between C2orf48 expression and the prognosis of patients with NPC was examined. Additionally, the effects of C2orf48 and high mobility group AT-hook 2 (HMGA2) upon NPC proliferation, migration, and invasion were examined employing the MTT assay, colony formation assay, and transwell assay, respectively. Furthermore, the association between C2orf48 and HMGA2 in NPC was investigated. Our research demonstrated that C2orf48 was overexpressed in NPC tissues and cell lines, and compared to patients with lower levels of C2orf48 expression, those with higher levels had poorer 5-year overall survival and progression-free survival. Functionally, C2orf48 overexpression accelerated NPC cells proliferation, migration, and invasion. Besides, the tandem mass tag (TMT) quantitative proteomic analysis indicated that HMGA2 may be a target of C2orf48. Moreover, upregulation of C2orf48 could increase HMGA2 expression, and HMGA2 silencing could counteract the proliferation, migration, and invasion changes induced by C2orf48 in NPC cells. These results reveal that overexpression of C2orf48 can promote NPC cells proliferation, migration, and invasion via regulating the expression of HMGA2 and C2orf48 may be a potentially important prognostic marker for NPC.</description><subject>Hematology</subject><subject>Internal Medicine</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>Pathology</subject><subject>Throat cancer</subject><issn>1559-131X</issn><issn>1357-0560</issn><issn>1559-131X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kE1LxDAQhoMouK7-AU8BL16qyWTbJsdl8QsWvKzgLaRp2mZtmzVpD_vvzW4FxYOHMBl43mHmQeiakjtKSH4fKBAGCQEWH81Fwk7QjKapSCij76e__ufoIoQtiVQKYoaaFThfLTjeede5wQQ8NObQ1N6EYF2PXYV7FdyuUX7f10a1WCuvbe86hYs99qYeWzXYvsaNrRvcucK2dtjj2rtxh5ebpHHuA8MlOqtUG8zVd52jt8eHzeo5Wb8-vayW60QzwoakUNSYhTaCZQQ0MWmhWVlUkDEoRS5AlxlPKRcFKytmMqAljyWHokr5gmjO5uh2mhtv-BxNGGRngzZtq3rjxiCBZyKjwCGP6M0fdOtG38ftjhQThIsDBROlvQvBm0ruvO2iDEmJPMiXk3wZ5cujfMliiE2hEOFozf-M_if1BaXUh7k</recordid><startdate>20230927</startdate><enddate>20230927</enddate><creator>Jiang, Yanhui</creator><creator>Liang, Faya</creator><creator>Chen, Renhui</creator><creator>Huang, Yongsheng</creator><creator>Xiao, Zhiwen</creator><creator>Zeng, Haicang</creator><creator>Han, Ping</creator><creator>Huang, Xiaoming</creator><general>Springer US</general><general>Springer Nature B.V</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>7X8</scope><orcidid>https://orcid.org/0000-0002-5859-533X</orcidid><orcidid>https://orcid.org/0000-0001-6097-7794</orcidid></search><sort><creationdate>20230927</creationdate><title>C2orf48 promotes the progression of nasopharyngeal carcinoma by regulating high mobility group AT-hook 2</title><author>Jiang, Yanhui ; Liang, Faya ; Chen, Renhui ; Huang, Yongsheng ; Xiao, Zhiwen ; Zeng, Haicang ; Han, Ping ; Huang, Xiaoming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c303t-ba1ee4ce93602c0e5bc3dbf2632d9792cd685189b3df3e621d83e672bf5840c83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Hematology</topic><topic>Internal Medicine</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><topic>Original Paper</topic><topic>Pathology</topic><topic>Throat cancer</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Yanhui</creatorcontrib><creatorcontrib>Liang, Faya</creatorcontrib><creatorcontrib>Chen, Renhui</creatorcontrib><creatorcontrib>Huang, Yongsheng</creatorcontrib><creatorcontrib>Xiao, Zhiwen</creatorcontrib><creatorcontrib>Zeng, Haicang</creatorcontrib><creatorcontrib>Han, Ping</creatorcontrib><creatorcontrib>Huang, Xiaoming</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health and Medical</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 UK/Ireland</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>PML(ProQuest Medical Library)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Medical oncology (Northwood, London, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Yanhui</au><au>Liang, Faya</au><au>Chen, Renhui</au><au>Huang, Yongsheng</au><au>Xiao, Zhiwen</au><au>Zeng, Haicang</au><au>Han, Ping</au><au>Huang, Xiaoming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C2orf48 promotes the progression of nasopharyngeal carcinoma by regulating high mobility group AT-hook 2</atitle><jtitle>Medical oncology (Northwood, London, England)</jtitle><stitle>Med Oncol</stitle><date>2023-09-27</date><risdate>2023</risdate><volume>40</volume><issue>11</issue><spage>306</spage><epage>306</epage><pages>306-306</pages><artnum>306</artnum><issn>1559-131X</issn><issn>1357-0560</issn><eissn>1559-131X</eissn><abstract>Recurrence and metastasis are the major factors affecting the survival of nasopharyngeal carcinoma (NPC), and the mechanism remains unclear. Long non-coding RNA chromosome 2 open reading frame 48 (C2orf48) has been shown to influence the prognosis of many cancers. However, C2orf48’s function in NPC has not been clarified. In this investigation, C2orf48 expression in NPC was measured by quantitative real-time PCR (qRT-PCR) at the cellular and tissue levels, and the association between C2orf48 expression and the prognosis of patients with NPC was examined. Additionally, the effects of C2orf48 and high mobility group AT-hook 2 (HMGA2) upon NPC proliferation, migration, and invasion were examined employing the MTT assay, colony formation assay, and transwell assay, respectively. Furthermore, the association between C2orf48 and HMGA2 in NPC was investigated. Our research demonstrated that C2orf48 was overexpressed in NPC tissues and cell lines, and compared to patients with lower levels of C2orf48 expression, those with higher levels had poorer 5-year overall survival and progression-free survival. Functionally, C2orf48 overexpression accelerated NPC cells proliferation, migration, and invasion. Besides, the tandem mass tag (TMT) quantitative proteomic analysis indicated that HMGA2 may be a target of C2orf48. Moreover, upregulation of C2orf48 could increase HMGA2 expression, and HMGA2 silencing could counteract the proliferation, migration, and invasion changes induced by C2orf48 in NPC cells. These results reveal that overexpression of C2orf48 can promote NPC cells proliferation, migration, and invasion via regulating the expression of HMGA2 and C2orf48 may be a potentially important prognostic marker for NPC.</abstract><cop>New York</cop><pub>Springer US</pub><doi>10.1007/s12032-023-02179-3</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-5859-533X</orcidid><orcidid>https://orcid.org/0000-0001-6097-7794</orcidid></addata></record> |
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title | C2orf48 promotes the progression of nasopharyngeal carcinoma by regulating high mobility group AT-hook 2 |
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