G9a Regulates Cell Sensitivity to Radiotherapy via Histone H3 Lysine 9 Trimethylation and CCDC8 in Lung Cancer
To investigate the role and underlying mechanism of G9a and CCDC8 in lung cancer radioresistance. Western blotting assays were used for G9a, CCDC8, H3K9me3 expression detection. MTT assays and clone formation assays were used for measuring cell proliferation activities. Flow cytometry assays were us...
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| Veröffentlicht in: | OncoTargets and therapy 2021-01, Vol.14, p.3721-3728 |
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| creator | Li, Yunfen Chen, Zhengting Cao, Ke Zhang, Lan Ma, Yuhui Yu, Shuhui Jin, Hanyu Liu, Xiaoling Li, Wenhui |
| description | To investigate the role and underlying mechanism of G9a and CCDC8 in lung cancer radioresistance.
Western blotting assays were used for G9a, CCDC8, H3K9me3 expression detection. MTT assays and clone formation assays were used for measuring cell proliferation activities. Flow cytometry assays were used for cell apoptosis detection. The enrichment of H3K9me3 in CCDC8 promoter was measured by chromatin immunoprecipitation assay.
G9a and G9a-mediated H3K9me3 are upregulated in radioresistant lung cancer cells (A549/IR cell and XWLC-05/IR cell). Blocking G9a not only promotes radiosensitivity of A549/IR cell and XWLC-05/IR cell but also reduces aggressive behavior of radioresistant A549 cell/IR and XWLC-05/IR cell. In addition, G9a-controlled H3K9me3 is able to binding to the promoter of tumor suppressor gene CCDC8 and suppresses CCDC8 expression. CCDC8 dysregulation is responsible for G9a-mediated radioresistance of A549/IR cell and XWLC-05/IR cell.
G9a and H3K9me3 contribute to the lung cancer radioresistance via modulating CCDC8 expression. |
| doi_str_mv | 10.2147/OTT.S296937 |
| format | Article |
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Western blotting assays were used for G9a, CCDC8, H3K9me3 expression detection. MTT assays and clone formation assays were used for measuring cell proliferation activities. Flow cytometry assays were used for cell apoptosis detection. The enrichment of H3K9me3 in CCDC8 promoter was measured by chromatin immunoprecipitation assay.
G9a and G9a-mediated H3K9me3 are upregulated in radioresistant lung cancer cells (A549/IR cell and XWLC-05/IR cell). Blocking G9a not only promotes radiosensitivity of A549/IR cell and XWLC-05/IR cell but also reduces aggressive behavior of radioresistant A549 cell/IR and XWLC-05/IR cell. In addition, G9a-controlled H3K9me3 is able to binding to the promoter of tumor suppressor gene CCDC8 and suppresses CCDC8 expression. CCDC8 dysregulation is responsible for G9a-mediated radioresistance of A549/IR cell and XWLC-05/IR cell.
G9a and H3K9me3 contribute to the lung cancer radioresistance via modulating CCDC8 expression.</description><identifier>ISSN: 1178-6930</identifier><identifier>EISSN: 1178-6930</identifier><identifier>DOI: 10.2147/OTT.S296937</identifier><identifier>PMID: 34140780</identifier><language>eng</language><publisher>New Zealand: Dove Medical Press Limited</publisher><subject>Antibodies ; Apoptosis ; Cancer therapies ; Cell growth ; Cell proliferation ; Chromatin ; Cloning ; DNA methylation ; Epigenetics ; Flow cytometry ; Genes ; Histone H3 ; Histones ; Immunoprecipitation ; Lung cancer ; Lysine ; Original Research ; Proteins ; Quantitative analysis ; Radiation therapy ; Radioresistance ; Radiosensitivity ; Radiotherapy ; Statistical analysis ; Tumor suppressor genes ; Western blotting</subject><ispartof>OncoTargets and therapy, 2021-01, Vol.14, p.3721-3728</ispartof><rights>2021 Li et al.</rights><rights>COPYRIGHT 2021 Dove Medical Press Limited</rights><rights>2021. This work is licensed under https://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 Li et al. 2021 Li et al.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c507t-f1d23b4caff469c3769bcdc2903ea9dc25f8292259780595f7c5e21e3cfbb553</citedby><cites>FETCH-LOGICAL-c507t-f1d23b4caff469c3769bcdc2903ea9dc25f8292259780595f7c5e21e3cfbb553</cites><orcidid>0000-0001-7461-2796 ; 0000-0003-3019-0450</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/PMC8203200/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8203200/$$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/34140780$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Yunfen</creatorcontrib><creatorcontrib>Chen, Zhengting</creatorcontrib><creatorcontrib>Cao, Ke</creatorcontrib><creatorcontrib>Zhang, Lan</creatorcontrib><creatorcontrib>Ma, Yuhui</creatorcontrib><creatorcontrib>Yu, Shuhui</creatorcontrib><creatorcontrib>Jin, Hanyu</creatorcontrib><creatorcontrib>Liu, Xiaoling</creatorcontrib><creatorcontrib>Li, Wenhui</creatorcontrib><title>G9a Regulates Cell Sensitivity to Radiotherapy via Histone H3 Lysine 9 Trimethylation and CCDC8 in Lung Cancer</title><title>OncoTargets and therapy</title><addtitle>Onco Targets Ther</addtitle><description>To investigate the role and underlying mechanism of G9a and CCDC8 in lung cancer radioresistance.
Western blotting assays were used for G9a, CCDC8, H3K9me3 expression detection. MTT assays and clone formation assays were used for measuring cell proliferation activities. Flow cytometry assays were used for cell apoptosis detection. The enrichment of H3K9me3 in CCDC8 promoter was measured by chromatin immunoprecipitation assay.
G9a and G9a-mediated H3K9me3 are upregulated in radioresistant lung cancer cells (A549/IR cell and XWLC-05/IR cell). Blocking G9a not only promotes radiosensitivity of A549/IR cell and XWLC-05/IR cell but also reduces aggressive behavior of radioresistant A549 cell/IR and XWLC-05/IR cell. In addition, G9a-controlled H3K9me3 is able to binding to the promoter of tumor suppressor gene CCDC8 and suppresses CCDC8 expression. CCDC8 dysregulation is responsible for G9a-mediated radioresistance of A549/IR cell and XWLC-05/IR cell.
G9a and H3K9me3 contribute to the lung cancer radioresistance via modulating CCDC8 expression.</description><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Chromatin</subject><subject>Cloning</subject><subject>DNA methylation</subject><subject>Epigenetics</subject><subject>Flow cytometry</subject><subject>Genes</subject><subject>Histone H3</subject><subject>Histones</subject><subject>Immunoprecipitation</subject><subject>Lung cancer</subject><subject>Lysine</subject><subject>Original Research</subject><subject>Proteins</subject><subject>Quantitative analysis</subject><subject>Radiation therapy</subject><subject>Radioresistance</subject><subject>Radiosensitivity</subject><subject>Radiotherapy</subject><subject>Statistical analysis</subject><subject>Tumor suppressor genes</subject><subject>Western blotting</subject><issn>1178-6930</issn><issn>1178-6930</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkl1r2zAUhs3YWD-2q90PwWAURjJ9WLZ1Myje1gwChdb3QpaPEhVHyiw54H8_mWYlGUMgvUjPeXV0dLLsA8FLSvLy633TLB-pKAQrX2WXhJTVImn8-kRfZFchPGFcFBXN32YXLCc5Lit8mbk7odADbMZeRQiohr5Hj-CCjfZg44SiRw-qsz5uYVD7CR2sQisboneAVgytp2CTEqgZ7A7idko21jukXIfq-ntdIevQenQbVCunYXiXvTGqD_D-uF5nzc8fTb1arO_vftW364XmuIwLQzrK2lwrY_JCaFYWotWdpgIzUCIJbioqKOUiPYILbkrNgRJg2rQt5-w6-_Zsux_bHXQaXBxUL_cpSTVM0isrz0-c3cqNP8iKYkYxTgY3R4PB_x4hRLmzQafiKAd-DJLynOU8LwuS0E__oE9-HFx63UyRqkjTCbVRPUjrjE_36tlU3hZlRQjBxZz38j9UGh3srE41NzbtnwV8PgnYgurjNvh-nD8hnINfnkE9-BAGMC_FIFjObSRTG8ljGyX642n9Xti_fcP-ACOpwAw</recordid><startdate>20210101</startdate><enddate>20210101</enddate><creator>Li, Yunfen</creator><creator>Chen, Zhengting</creator><creator>Cao, Ke</creator><creator>Zhang, Lan</creator><creator>Ma, Yuhui</creator><creator>Yu, Shuhui</creator><creator>Jin, Hanyu</creator><creator>Liu, Xiaoling</creator><creator>Li, Wenhui</creator><general>Dove Medical Press Limited</general><general>Taylor & Francis Ltd</general><general>Dove</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</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>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7461-2796</orcidid><orcidid>https://orcid.org/0000-0003-3019-0450</orcidid></search><sort><creationdate>20210101</creationdate><title>G9a Regulates Cell Sensitivity to Radiotherapy via Histone H3 Lysine 9 Trimethylation and CCDC8 in Lung Cancer</title><author>Li, Yunfen ; Chen, Zhengting ; Cao, Ke ; Zhang, Lan ; Ma, Yuhui ; Yu, Shuhui ; Jin, Hanyu ; Liu, Xiaoling ; Li, Wenhui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-f1d23b4caff469c3769bcdc2903ea9dc25f8292259780595f7c5e21e3cfbb553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Cancer therapies</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Chromatin</topic><topic>Cloning</topic><topic>DNA methylation</topic><topic>Epigenetics</topic><topic>Flow cytometry</topic><topic>Genes</topic><topic>Histone H3</topic><topic>Histones</topic><topic>Immunoprecipitation</topic><topic>Lung cancer</topic><topic>Lysine</topic><topic>Original Research</topic><topic>Proteins</topic><topic>Quantitative analysis</topic><topic>Radiation therapy</topic><topic>Radioresistance</topic><topic>Radiosensitivity</topic><topic>Radiotherapy</topic><topic>Statistical analysis</topic><topic>Tumor suppressor genes</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Yunfen</creatorcontrib><creatorcontrib>Chen, Zhengting</creatorcontrib><creatorcontrib>Cao, Ke</creatorcontrib><creatorcontrib>Zhang, Lan</creatorcontrib><creatorcontrib>Ma, Yuhui</creatorcontrib><creatorcontrib>Yu, Shuhui</creatorcontrib><creatorcontrib>Jin, Hanyu</creatorcontrib><creatorcontrib>Liu, Xiaoling</creatorcontrib><creatorcontrib>Li, Wenhui</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>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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</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>Research Library Prep</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>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Access via ProQuest (Open Access)</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>ProQuest Central Basic</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>Li, Yunfen</au><au>Chen, Zhengting</au><au>Cao, Ke</au><au>Zhang, Lan</au><au>Ma, Yuhui</au><au>Yu, Shuhui</au><au>Jin, Hanyu</au><au>Liu, Xiaoling</au><au>Li, Wenhui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>G9a Regulates Cell Sensitivity to Radiotherapy via Histone H3 Lysine 9 Trimethylation and CCDC8 in Lung Cancer</atitle><jtitle>OncoTargets and therapy</jtitle><addtitle>Onco Targets Ther</addtitle><date>2021-01-01</date><risdate>2021</risdate><volume>14</volume><spage>3721</spage><epage>3728</epage><pages>3721-3728</pages><issn>1178-6930</issn><eissn>1178-6930</eissn><abstract>To investigate the role and underlying mechanism of G9a and CCDC8 in lung cancer radioresistance.
Western blotting assays were used for G9a, CCDC8, H3K9me3 expression detection. MTT assays and clone formation assays were used for measuring cell proliferation activities. Flow cytometry assays were used for cell apoptosis detection. The enrichment of H3K9me3 in CCDC8 promoter was measured by chromatin immunoprecipitation assay.
G9a and G9a-mediated H3K9me3 are upregulated in radioresistant lung cancer cells (A549/IR cell and XWLC-05/IR cell). Blocking G9a not only promotes radiosensitivity of A549/IR cell and XWLC-05/IR cell but also reduces aggressive behavior of radioresistant A549 cell/IR and XWLC-05/IR cell. In addition, G9a-controlled H3K9me3 is able to binding to the promoter of tumor suppressor gene CCDC8 and suppresses CCDC8 expression. CCDC8 dysregulation is responsible for G9a-mediated radioresistance of A549/IR cell and XWLC-05/IR cell.
G9a and H3K9me3 contribute to the lung cancer radioresistance via modulating CCDC8 expression.</abstract><cop>New Zealand</cop><pub>Dove Medical Press Limited</pub><pmid>34140780</pmid><doi>10.2147/OTT.S296937</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-7461-2796</orcidid><orcidid>https://orcid.org/0000-0003-3019-0450</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antibodies Apoptosis Cancer therapies Cell growth Cell proliferation Chromatin Cloning DNA methylation Epigenetics Flow cytometry Genes Histone H3 Histones Immunoprecipitation Lung cancer Lysine Original Research Proteins Quantitative analysis Radiation therapy Radioresistance Radiosensitivity Radiotherapy Statistical analysis Tumor suppressor genes Western blotting |
| title | G9a Regulates Cell Sensitivity to Radiotherapy via Histone H3 Lysine 9 Trimethylation and CCDC8 in Lung Cancer |
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