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Hypermethylation of GNA14 and its tumor-suppressive role in hepatitis B virus-related hepatocellular carcinoma
Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide, and its specific mechanism has not been fully elucidated. Inactivation of tumor suppressors may contribute to the occurrence, progression, and recurrence of HCC. DNA methylation is a crucial mechanism involved in regulating...
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| Published in: | Theranostics 2021, Vol.11 (5), p.2318-2333 |
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| creator | Song, Guangyuan Zhu, Xingxin Xuan, Zefeng Zhao, Long Dong, Haijiang Chen, Jian Li, Zequn Song, Wenfeng Jin, Cheng Zhou, Mengqiao Xie, Haiyang Zheng, Shusen Song, Penghong |
| description | Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide, and its specific mechanism has not been fully elucidated. Inactivation of tumor suppressors may contribute to the occurrence, progression, and recurrence of HCC. DNA methylation is a crucial mechanism involved in regulating the occurrence of HCC. Herein, we aimed to identify the key methylation-related tumor suppressors as well as potential biomarkers and therapeutic targets in HCC.
: Combined analysis of TCGA and GEO databases was performed to obtain potential methylation-related tumor suppressors in HCC. Methyl-target sequencing was performed to analyze the methylation level of the GNA14 promoter. The diagnostic value of GNA14 as a predictor of HCC was evaluated in HCC tumor samples and compared with normal tissues. The functional role of GNA14 and its upstream and downstream regulatory factors were investigated by gain-of-function and loss-of-function assays
. Subcutaneous tumorigenesis, lung colonization, and orthotopic liver tumor model were performed to analyze the role of GNA14
: The expression of GNA14 was found to be downregulated in HCC and it was negatively correlated with hepatitis B virus (HBV) infection, vascular invasion, and prognosis of HCC. DNA methylation was demonstrated to be responsible for the altered expression of GNA14 and was regulated by HBV-encoded X protein (HBx). GNA14 regulated the RB pathway by promoting Notch1 cleavage to inhibit tumor proliferation, and might inhibit tumor metastasis by inhibiting the expression of JMJD6.
: GNA14 could be regulated by HBx by modulating the methylation status of its promoter. We identified GNA14 as a potential biomarker and therapeutic target for HCC. |
| doi_str_mv | 10.7150/thno.48739 |
| format | article |
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: Combined analysis of TCGA and GEO databases was performed to obtain potential methylation-related tumor suppressors in HCC. Methyl-target sequencing was performed to analyze the methylation level of the GNA14 promoter. The diagnostic value of GNA14 as a predictor of HCC was evaluated in HCC tumor samples and compared with normal tissues. The functional role of GNA14 and its upstream and downstream regulatory factors were investigated by gain-of-function and loss-of-function assays
. Subcutaneous tumorigenesis, lung colonization, and orthotopic liver tumor model were performed to analyze the role of GNA14
: The expression of GNA14 was found to be downregulated in HCC and it was negatively correlated with hepatitis B virus (HBV) infection, vascular invasion, and prognosis of HCC. DNA methylation was demonstrated to be responsible for the altered expression of GNA14 and was regulated by HBV-encoded X protein (HBx). GNA14 regulated the RB pathway by promoting Notch1 cleavage to inhibit tumor proliferation, and might inhibit tumor metastasis by inhibiting the expression of JMJD6.
: GNA14 could be regulated by HBx by modulating the methylation status of its promoter. We identified GNA14 as a potential biomarker and therapeutic target for HCC.</description><identifier>ISSN: 1838-7640</identifier><identifier>EISSN: 1838-7640</identifier><identifier>DOI: 10.7150/thno.48739</identifier><identifier>PMID: 33500727</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>Cell culture ; Cell growth ; DNA methylation ; Genes ; Hepatitis B ; Hospitals ; Infections ; Liver cancer ; Medicine ; Metastasis ; Proteins ; Research Paper ; Signal transduction ; Tumors</subject><ispartof>Theranostics, 2021, Vol.11 (5), p.2318-2333</ispartof><rights>The author(s).</rights><rights>2021. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The author(s) 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-ac87e77d1bc327444bbc825928003635d5ed4c689838f1566a0b3c7a317e29e83</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2598242960/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2598242960?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4009,25732,27902,27903,27904,36991,36992,44569,53769,53771,74872</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33500727$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Song, Guangyuan</creatorcontrib><creatorcontrib>Zhu, Xingxin</creatorcontrib><creatorcontrib>Xuan, Zefeng</creatorcontrib><creatorcontrib>Zhao, Long</creatorcontrib><creatorcontrib>Dong, Haijiang</creatorcontrib><creatorcontrib>Chen, Jian</creatorcontrib><creatorcontrib>Li, Zequn</creatorcontrib><creatorcontrib>Song, Wenfeng</creatorcontrib><creatorcontrib>Jin, Cheng</creatorcontrib><creatorcontrib>Zhou, Mengqiao</creatorcontrib><creatorcontrib>Xie, Haiyang</creatorcontrib><creatorcontrib>Zheng, Shusen</creatorcontrib><creatorcontrib>Song, Penghong</creatorcontrib><title>Hypermethylation of GNA14 and its tumor-suppressive role in hepatitis B virus-related hepatocellular carcinoma</title><title>Theranostics</title><addtitle>Theranostics</addtitle><description>Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide, and its specific mechanism has not been fully elucidated. Inactivation of tumor suppressors may contribute to the occurrence, progression, and recurrence of HCC. DNA methylation is a crucial mechanism involved in regulating the occurrence of HCC. Herein, we aimed to identify the key methylation-related tumor suppressors as well as potential biomarkers and therapeutic targets in HCC.
: Combined analysis of TCGA and GEO databases was performed to obtain potential methylation-related tumor suppressors in HCC. Methyl-target sequencing was performed to analyze the methylation level of the GNA14 promoter. The diagnostic value of GNA14 as a predictor of HCC was evaluated in HCC tumor samples and compared with normal tissues. The functional role of GNA14 and its upstream and downstream regulatory factors were investigated by gain-of-function and loss-of-function assays
. Subcutaneous tumorigenesis, lung colonization, and orthotopic liver tumor model were performed to analyze the role of GNA14
: The expression of GNA14 was found to be downregulated in HCC and it was negatively correlated with hepatitis B virus (HBV) infection, vascular invasion, and prognosis of HCC. DNA methylation was demonstrated to be responsible for the altered expression of GNA14 and was regulated by HBV-encoded X protein (HBx). GNA14 regulated the RB pathway by promoting Notch1 cleavage to inhibit tumor proliferation, and might inhibit tumor metastasis by inhibiting the expression of JMJD6.
: GNA14 could be regulated by HBx by modulating the methylation status of its promoter. We identified GNA14 as a potential biomarker and therapeutic target for HCC.</description><subject>Cell culture</subject><subject>Cell growth</subject><subject>DNA methylation</subject><subject>Genes</subject><subject>Hepatitis B</subject><subject>Hospitals</subject><subject>Infections</subject><subject>Liver cancer</subject><subject>Medicine</subject><subject>Metastasis</subject><subject>Proteins</subject><subject>Research Paper</subject><subject>Signal transduction</subject><subject>Tumors</subject><issn>1838-7640</issn><issn>1838-7640</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNpdkc1rFTEUxYMottRu_AMk4EaEqfmafGyEtmgrFN3oOmQy9_lSZpIxyTx4_715vlqq2dzA_d3DORyEXlNyoWhPPtRtTBdCK26eoVOque6UFOT5k_8JOi_lnrQnCDPUvEQnnPeEKKZOUbzdL5BnqNv95GpIEacNvvl6SQV2ccShFlzXOeWurMuSoZSwA5zTBDhEvIWl3dRQ8BXehbyWLkNTgfG4SR6maZ1cxt5lH2Ka3Sv0YuOmAucP8wz9-Pzp-_Vtd_ft5sv15V3nBZG1c14rUGqkg-dMCSGGwWvWG6YJ4ZL3Yw-j8FKblnFDeykdGbhXjlMFzIDmZ-jjUXdZhxlGD7FmN9klh9nlvU0u2H83MWztz7SzShklDWkC7x4Ecvq1Qql2DuWQx0VIa7FMaCp7wrlp6Nv_0Pu05tji2WZZM8GMPAi-P1I-p1IybB7NUGIPTdpDk_ZPkw1-89T-I_q3N_4bz1Ga-g</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Song, Guangyuan</creator><creator>Zhu, Xingxin</creator><creator>Xuan, Zefeng</creator><creator>Zhao, Long</creator><creator>Dong, Haijiang</creator><creator>Chen, Jian</creator><creator>Li, Zequn</creator><creator>Song, Wenfeng</creator><creator>Jin, Cheng</creator><creator>Zhou, Mengqiao</creator><creator>Xie, Haiyang</creator><creator>Zheng, Shusen</creator><creator>Song, Penghong</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>2021</creationdate><title>Hypermethylation of GNA14 and its tumor-suppressive role in hepatitis B virus-related hepatocellular carcinoma</title><author>Song, Guangyuan ; Zhu, Xingxin ; Xuan, Zefeng ; Zhao, Long ; Dong, Haijiang ; Chen, Jian ; Li, Zequn ; Song, Wenfeng ; Jin, Cheng ; Zhou, Mengqiao ; Xie, Haiyang ; Zheng, Shusen ; Song, Penghong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c406t-ac87e77d1bc327444bbc825928003635d5ed4c689838f1566a0b3c7a317e29e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Cell culture</topic><topic>Cell growth</topic><topic>DNA methylation</topic><topic>Genes</topic><topic>Hepatitis B</topic><topic>Hospitals</topic><topic>Infections</topic><topic>Liver cancer</topic><topic>Medicine</topic><topic>Metastasis</topic><topic>Proteins</topic><topic>Research Paper</topic><topic>Signal transduction</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Song, Guangyuan</creatorcontrib><creatorcontrib>Zhu, Xingxin</creatorcontrib><creatorcontrib>Xuan, Zefeng</creatorcontrib><creatorcontrib>Zhao, Long</creatorcontrib><creatorcontrib>Dong, Haijiang</creatorcontrib><creatorcontrib>Chen, Jian</creatorcontrib><creatorcontrib>Li, Zequn</creatorcontrib><creatorcontrib>Song, Wenfeng</creatorcontrib><creatorcontrib>Jin, Cheng</creatorcontrib><creatorcontrib>Zhou, Mengqiao</creatorcontrib><creatorcontrib>Xie, Haiyang</creatorcontrib><creatorcontrib>Zheng, Shusen</creatorcontrib><creatorcontrib>Song, Penghong</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>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</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</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>Publicly Available Content (ProQuest)</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>Theranostics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Song, Guangyuan</au><au>Zhu, Xingxin</au><au>Xuan, Zefeng</au><au>Zhao, Long</au><au>Dong, Haijiang</au><au>Chen, Jian</au><au>Li, Zequn</au><au>Song, Wenfeng</au><au>Jin, Cheng</au><au>Zhou, Mengqiao</au><au>Xie, Haiyang</au><au>Zheng, Shusen</au><au>Song, Penghong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypermethylation of GNA14 and its tumor-suppressive role in hepatitis B virus-related hepatocellular carcinoma</atitle><jtitle>Theranostics</jtitle><addtitle>Theranostics</addtitle><date>2021</date><risdate>2021</risdate><volume>11</volume><issue>5</issue><spage>2318</spage><epage>2333</epage><pages>2318-2333</pages><issn>1838-7640</issn><eissn>1838-7640</eissn><abstract>Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide, and its specific mechanism has not been fully elucidated. Inactivation of tumor suppressors may contribute to the occurrence, progression, and recurrence of HCC. DNA methylation is a crucial mechanism involved in regulating the occurrence of HCC. Herein, we aimed to identify the key methylation-related tumor suppressors as well as potential biomarkers and therapeutic targets in HCC.
: Combined analysis of TCGA and GEO databases was performed to obtain potential methylation-related tumor suppressors in HCC. Methyl-target sequencing was performed to analyze the methylation level of the GNA14 promoter. The diagnostic value of GNA14 as a predictor of HCC was evaluated in HCC tumor samples and compared with normal tissues. The functional role of GNA14 and its upstream and downstream regulatory factors were investigated by gain-of-function and loss-of-function assays
. Subcutaneous tumorigenesis, lung colonization, and orthotopic liver tumor model were performed to analyze the role of GNA14
: The expression of GNA14 was found to be downregulated in HCC and it was negatively correlated with hepatitis B virus (HBV) infection, vascular invasion, and prognosis of HCC. DNA methylation was demonstrated to be responsible for the altered expression of GNA14 and was regulated by HBV-encoded X protein (HBx). GNA14 regulated the RB pathway by promoting Notch1 cleavage to inhibit tumor proliferation, and might inhibit tumor metastasis by inhibiting the expression of JMJD6.
: GNA14 could be regulated by HBx by modulating the methylation status of its promoter. We identified GNA14 as a potential biomarker and therapeutic target for HCC.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>33500727</pmid><doi>10.7150/thno.48739</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Cell culture Cell growth DNA methylation Genes Hepatitis B Hospitals Infections Liver cancer Medicine Metastasis Proteins Research Paper Signal transduction Tumors |
| title | Hypermethylation of GNA14 and its tumor-suppressive role in hepatitis B virus-related hepatocellular carcinoma |
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