Long non‐coding RNA PANDAR promoted radiation and cisplatin‐induced DNA damage repair through ATR/CHK1 in NSCLC
Background DNA‐damaging agents, including radiation and platinum‐based chemotherapy, are indispensable treatments for non‐small cell lung cancer (NSCLC) patients. However, cancer cells tend to be resistant to both radiation and chemotherapy, thus resulting in treatment failure or recurrence. The pur...
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| creator | Zhao, Songyun Yu, Nanxi Wang, Hang Wan, Zhijie Diao, Chaoyue Chen, Yuanyuan Liu, Tingting Yang, Yanyong Gao, Fu Bai, Chong Cao, Kun Cai, Jianming |
| description | Background
DNA‐damaging agents, including radiation and platinum‐based chemotherapy, are indispensable treatments for non‐small cell lung cancer (NSCLC) patients. However, cancer cells tend to be resistant to both radiation and chemotherapy, thus resulting in treatment failure or recurrence. The purpose of this study was to explore the effect and mechanism of long non‐coding RNA (lncRNA) PANDAR (promoter of CDKN1A antisense DNA damage‐activated RNA) on NSCLC sensitivity to radiation and chemotherapy.
Methods
Cell counting kit (CCK‐8), colony formation and flow cytometry were respectively performed to determine the cell cycle and apoptosis of NSCLC cells treated with γ‐ray radiation and cisplatin. The extent of DNA damage was evaluated using a comet assay and immunofluorescence staining against γH2AX. In addition, we explored the role of PANDAR in DNA damage response pathways through western blot analysis. Finally, a nude mouse subcutaneous xenograft model was established to assess the sensitivity to radiation and chemotherapy in vivo.
Results
In cell experiments, PANDAR knockdown can increase the sensitivity of NSCLC cells to radiation and cisplatin. The CCK‐8 results showed that cell viability was significantly increased in the overexpression group after radiation and cisplatin treatments. The overexpression group also showed more colonies, less apoptosis and DNA damage, and G2/M phase arrest was aggravated to provide the time necessary for DNA repair. Contrary to PANDAR overexpression, the trends were reversed in the PANDAR knockdown group. Furthermore, PANDAR knockdown inhibited radiation and cisplatin‐activated phosphorylation levels of ATR and CHK1 in NSCLC cells. Finally, our in vivo model showed that targeting PANDAR significantly sensitized NSCLC to radiation and cisplatin.
Conclusion
Our study showed that PANDAR knockdown promoted sensitivity to radiation and cisplatin in NSCLC by regulating the ATR/CHK1 pathway, thus providing a novel understanding as well as a therapeutic target for NSCLC treatment.
In NSCLC cells, lncRNA PANDAR negatively regulates sensitivity to radiation and cisplatin. PANDAR can promote the repair of radiation and cisplatin‐induced DNA damage and activation of the G2/M checkpoint through the ATR/CHK1 pathway. PANDAR knockdown results in defects in DNA damage repair accompanied by more cell apoptosis.
In non‐small cell lung cancer (NSCLC) cells, lncRNA PANDAR negatively regulates sensitivity to radiation and cisplatin. PANDAR |
| doi_str_mv | 10.1002/jgm.3565 |
| format | Article |
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DNA‐damaging agents, including radiation and platinum‐based chemotherapy, are indispensable treatments for non‐small cell lung cancer (NSCLC) patients. However, cancer cells tend to be resistant to both radiation and chemotherapy, thus resulting in treatment failure or recurrence. The purpose of this study was to explore the effect and mechanism of long non‐coding RNA (lncRNA) PANDAR (promoter of CDKN1A antisense DNA damage‐activated RNA) on NSCLC sensitivity to radiation and chemotherapy.
Methods
Cell counting kit (CCK‐8), colony formation and flow cytometry were respectively performed to determine the cell cycle and apoptosis of NSCLC cells treated with γ‐ray radiation and cisplatin. The extent of DNA damage was evaluated using a comet assay and immunofluorescence staining against γH2AX. In addition, we explored the role of PANDAR in DNA damage response pathways through western blot analysis. Finally, a nude mouse subcutaneous xenograft model was established to assess the sensitivity to radiation and chemotherapy in vivo.
Results
In cell experiments, PANDAR knockdown can increase the sensitivity of NSCLC cells to radiation and cisplatin. The CCK‐8 results showed that cell viability was significantly increased in the overexpression group after radiation and cisplatin treatments. The overexpression group also showed more colonies, less apoptosis and DNA damage, and G2/M phase arrest was aggravated to provide the time necessary for DNA repair. Contrary to PANDAR overexpression, the trends were reversed in the PANDAR knockdown group. Furthermore, PANDAR knockdown inhibited radiation and cisplatin‐activated phosphorylation levels of ATR and CHK1 in NSCLC cells. Finally, our in vivo model showed that targeting PANDAR significantly sensitized NSCLC to radiation and cisplatin.
Conclusion
Our study showed that PANDAR knockdown promoted sensitivity to radiation and cisplatin in NSCLC by regulating the ATR/CHK1 pathway, thus providing a novel understanding as well as a therapeutic target for NSCLC treatment.
In NSCLC cells, lncRNA PANDAR negatively regulates sensitivity to radiation and cisplatin. PANDAR can promote the repair of radiation and cisplatin‐induced DNA damage and activation of the G2/M checkpoint through the ATR/CHK1 pathway. PANDAR knockdown results in defects in DNA damage repair accompanied by more cell apoptosis.
In non‐small cell lung cancer (NSCLC) cells, lncRNA PANDAR negatively regulates sensitivity to radiation and cisplatin. PANDAR can promote the repair of radiation and cisplatin‐induced DNA damage and activation of the G2/M checkpoint through the ATR/CHK1 pathway. PANDAR knockdown results in defects in DNA damage repair accompanied by more cell apoptosis.</description><identifier>ISSN: 1099-498X</identifier><identifier>EISSN: 1521-2254</identifier><identifier>DOI: 10.1002/jgm.3565</identifier><identifier>PMID: 37460393</identifier><language>eng</language><publisher>England: Wiley Periodicals Inc</publisher><subject>Animals ; Antisense DNA ; Antisense RNA ; Apoptosis ; Apoptosis - genetics ; Ataxia Telangiectasia Mutated Proteins - genetics ; Ataxia Telangiectasia Mutated Proteins - metabolism ; Ataxia Telangiectasia Mutated Proteins - therapeutic use ; cancer ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - therapy ; Cell cycle ; Cell Line, Tumor ; Cell Proliferation - genetics ; Cell viability ; cell‐therapy ; Chemotherapy ; CHK1 protein ; Cholecystokinin ; Cisplatin ; Cisplatin - pharmacology ; Comet assay ; DNA Damage ; DNA repair ; DNA Repair - genetics ; Flow cytometry ; Humans ; Immunofluorescence ; lung ; Lung cancer ; Lung Neoplasms - drug therapy ; Lung Neoplasms - therapy ; Mice ; molecular‐genetics ; Non-coding RNA ; Non-small cell lung carcinoma ; Phosphorylation ; Radiation ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Small cell lung carcinoma ; Therapeutic targets ; tumor therapy</subject><ispartof>The journal of gene medicine, 2023-12, Vol.25 (12), p.e3565-n/a</ispartof><rights>2023 John Wiley & Sons Ltd.</rights><rights>2023 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3105-3b513fb24a65d5ad10acab17c118cc614ed1184714dc4cd286e70fda26cc50483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjgm.3565$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjgm.3565$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37460393$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Songyun</creatorcontrib><creatorcontrib>Yu, Nanxi</creatorcontrib><creatorcontrib>Wang, Hang</creatorcontrib><creatorcontrib>Wan, Zhijie</creatorcontrib><creatorcontrib>Diao, Chaoyue</creatorcontrib><creatorcontrib>Chen, Yuanyuan</creatorcontrib><creatorcontrib>Liu, Tingting</creatorcontrib><creatorcontrib>Yang, Yanyong</creatorcontrib><creatorcontrib>Gao, Fu</creatorcontrib><creatorcontrib>Bai, Chong</creatorcontrib><creatorcontrib>Cao, Kun</creatorcontrib><creatorcontrib>Cai, Jianming</creatorcontrib><title>Long non‐coding RNA PANDAR promoted radiation and cisplatin‐induced DNA damage repair through ATR/CHK1 in NSCLC</title><title>The journal of gene medicine</title><addtitle>J Gene Med</addtitle><description>Background
DNA‐damaging agents, including radiation and platinum‐based chemotherapy, are indispensable treatments for non‐small cell lung cancer (NSCLC) patients. However, cancer cells tend to be resistant to both radiation and chemotherapy, thus resulting in treatment failure or recurrence. The purpose of this study was to explore the effect and mechanism of long non‐coding RNA (lncRNA) PANDAR (promoter of CDKN1A antisense DNA damage‐activated RNA) on NSCLC sensitivity to radiation and chemotherapy.
Methods
Cell counting kit (CCK‐8), colony formation and flow cytometry were respectively performed to determine the cell cycle and apoptosis of NSCLC cells treated with γ‐ray radiation and cisplatin. The extent of DNA damage was evaluated using a comet assay and immunofluorescence staining against γH2AX. In addition, we explored the role of PANDAR in DNA damage response pathways through western blot analysis. Finally, a nude mouse subcutaneous xenograft model was established to assess the sensitivity to radiation and chemotherapy in vivo.
Results
In cell experiments, PANDAR knockdown can increase the sensitivity of NSCLC cells to radiation and cisplatin. The CCK‐8 results showed that cell viability was significantly increased in the overexpression group after radiation and cisplatin treatments. The overexpression group also showed more colonies, less apoptosis and DNA damage, and G2/M phase arrest was aggravated to provide the time necessary for DNA repair. Contrary to PANDAR overexpression, the trends were reversed in the PANDAR knockdown group. Furthermore, PANDAR knockdown inhibited radiation and cisplatin‐activated phosphorylation levels of ATR and CHK1 in NSCLC cells. Finally, our in vivo model showed that targeting PANDAR significantly sensitized NSCLC to radiation and cisplatin.
Conclusion
Our study showed that PANDAR knockdown promoted sensitivity to radiation and cisplatin in NSCLC by regulating the ATR/CHK1 pathway, thus providing a novel understanding as well as a therapeutic target for NSCLC treatment.
In NSCLC cells, lncRNA PANDAR negatively regulates sensitivity to radiation and cisplatin. PANDAR can promote the repair of radiation and cisplatin‐induced DNA damage and activation of the G2/M checkpoint through the ATR/CHK1 pathway. PANDAR knockdown results in defects in DNA damage repair accompanied by more cell apoptosis.
In non‐small cell lung cancer (NSCLC) cells, lncRNA PANDAR negatively regulates sensitivity to radiation and cisplatin. PANDAR can promote the repair of radiation and cisplatin‐induced DNA damage and activation of the G2/M checkpoint through the ATR/CHK1 pathway. PANDAR knockdown results in defects in DNA damage repair accompanied by more cell apoptosis.</description><subject>Animals</subject><subject>Antisense DNA</subject><subject>Antisense RNA</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Ataxia Telangiectasia Mutated Proteins - genetics</subject><subject>Ataxia Telangiectasia Mutated Proteins - metabolism</subject><subject>Ataxia Telangiectasia Mutated Proteins - therapeutic use</subject><subject>cancer</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - therapy</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Cell viability</subject><subject>cell‐therapy</subject><subject>Chemotherapy</subject><subject>CHK1 protein</subject><subject>Cholecystokinin</subject><subject>Cisplatin</subject><subject>Cisplatin - pharmacology</subject><subject>Comet assay</subject><subject>DNA Damage</subject><subject>DNA repair</subject><subject>DNA Repair - genetics</subject><subject>Flow cytometry</subject><subject>Humans</subject><subject>Immunofluorescence</subject><subject>lung</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - therapy</subject><subject>Mice</subject><subject>molecular‐genetics</subject><subject>Non-coding RNA</subject><subject>Non-small cell lung carcinoma</subject><subject>Phosphorylation</subject><subject>Radiation</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Small cell lung carcinoma</subject><subject>Therapeutic targets</subject><subject>tumor therapy</subject><issn>1099-498X</issn><issn>1521-2254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctOGzEUhi1EBSmtxBMgS2zYDPg6l-VoKKEQQpWCxM5ybCdxNGOndkZVdn2EPmOfBIdLkZDwxudI3_l07B-AQ4xOMULkbDnvTinP-Q4YYE5wRghnu6lGVZWxqnzYB59jXCKEi7Ks9sA-LViOaEUHII68m0Pn3b8_f5XXNjWTcQ1_1OPzegJXwXd-bTQMUlu5tt5B6TRUNq7a1G6HrNO9SsR5mtKyk3MDg1lJG-B6EXw_X8D6bnLWXF5jaB0c_2xGzRfwaSbbaL6-3Afg_uLbXXOZjW6H35t6lCmKEc_olGM6mxImc6651BhJJae4UBiXSuWYGZ0qVmCmFVOalLkp0ExLkivFESvpATh59qZn_OpNXIvORmXaVjrj-yhISSvCqnQSevwOXfo-uLSdIBWiqCgQom9CFXyMwczEKthOho3ASGyDECkIsQ0ioUcvwn7aGf0ffP35BGTPwG_bms2HInE1vHkSPgI8QJEE</recordid><startdate>202312</startdate><enddate>202312</enddate><creator>Zhao, Songyun</creator><creator>Yu, Nanxi</creator><creator>Wang, Hang</creator><creator>Wan, Zhijie</creator><creator>Diao, Chaoyue</creator><creator>Chen, Yuanyuan</creator><creator>Liu, Tingting</creator><creator>Yang, Yanyong</creator><creator>Gao, Fu</creator><creator>Bai, Chong</creator><creator>Cao, Kun</creator><creator>Cai, Jianming</creator><general>Wiley Periodicals Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>202312</creationdate><title>Long non‐coding RNA PANDAR promoted radiation and cisplatin‐induced DNA damage repair through ATR/CHK1 in NSCLC</title><author>Zhao, Songyun ; Yu, Nanxi ; Wang, Hang ; Wan, Zhijie ; Diao, Chaoyue ; Chen, Yuanyuan ; Liu, Tingting ; Yang, Yanyong ; Gao, Fu ; Bai, Chong ; Cao, Kun ; Cai, Jianming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3105-3b513fb24a65d5ad10acab17c118cc614ed1184714dc4cd286e70fda26cc50483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Antisense DNA</topic><topic>Antisense RNA</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Ataxia Telangiectasia Mutated Proteins - genetics</topic><topic>Ataxia Telangiectasia Mutated Proteins - metabolism</topic><topic>Ataxia Telangiectasia Mutated Proteins - therapeutic use</topic><topic>cancer</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - therapy</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Cell viability</topic><topic>cell‐therapy</topic><topic>Chemotherapy</topic><topic>CHK1 protein</topic><topic>Cholecystokinin</topic><topic>Cisplatin</topic><topic>Cisplatin - pharmacology</topic><topic>Comet assay</topic><topic>DNA Damage</topic><topic>DNA repair</topic><topic>DNA Repair - genetics</topic><topic>Flow cytometry</topic><topic>Humans</topic><topic>Immunofluorescence</topic><topic>lung</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - therapy</topic><topic>Mice</topic><topic>molecular‐genetics</topic><topic>Non-coding RNA</topic><topic>Non-small cell lung carcinoma</topic><topic>Phosphorylation</topic><topic>Radiation</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Small cell lung carcinoma</topic><topic>Therapeutic targets</topic><topic>tumor therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Songyun</creatorcontrib><creatorcontrib>Yu, Nanxi</creatorcontrib><creatorcontrib>Wang, Hang</creatorcontrib><creatorcontrib>Wan, Zhijie</creatorcontrib><creatorcontrib>Diao, Chaoyue</creatorcontrib><creatorcontrib>Chen, Yuanyuan</creatorcontrib><creatorcontrib>Liu, Tingting</creatorcontrib><creatorcontrib>Yang, Yanyong</creatorcontrib><creatorcontrib>Gao, Fu</creatorcontrib><creatorcontrib>Bai, Chong</creatorcontrib><creatorcontrib>Cao, Kun</creatorcontrib><creatorcontrib>Cai, Jianming</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The journal of gene medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Songyun</au><au>Yu, Nanxi</au><au>Wang, Hang</au><au>Wan, Zhijie</au><au>Diao, Chaoyue</au><au>Chen, Yuanyuan</au><au>Liu, Tingting</au><au>Yang, Yanyong</au><au>Gao, Fu</au><au>Bai, Chong</au><au>Cao, Kun</au><au>Cai, Jianming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long non‐coding RNA PANDAR promoted radiation and cisplatin‐induced DNA damage repair through ATR/CHK1 in NSCLC</atitle><jtitle>The journal of gene medicine</jtitle><addtitle>J Gene Med</addtitle><date>2023-12</date><risdate>2023</risdate><volume>25</volume><issue>12</issue><spage>e3565</spage><epage>n/a</epage><pages>e3565-n/a</pages><issn>1099-498X</issn><eissn>1521-2254</eissn><abstract>Background
DNA‐damaging agents, including radiation and platinum‐based chemotherapy, are indispensable treatments for non‐small cell lung cancer (NSCLC) patients. However, cancer cells tend to be resistant to both radiation and chemotherapy, thus resulting in treatment failure or recurrence. The purpose of this study was to explore the effect and mechanism of long non‐coding RNA (lncRNA) PANDAR (promoter of CDKN1A antisense DNA damage‐activated RNA) on NSCLC sensitivity to radiation and chemotherapy.
Methods
Cell counting kit (CCK‐8), colony formation and flow cytometry were respectively performed to determine the cell cycle and apoptosis of NSCLC cells treated with γ‐ray radiation and cisplatin. The extent of DNA damage was evaluated using a comet assay and immunofluorescence staining against γH2AX. In addition, we explored the role of PANDAR in DNA damage response pathways through western blot analysis. Finally, a nude mouse subcutaneous xenograft model was established to assess the sensitivity to radiation and chemotherapy in vivo.
Results
In cell experiments, PANDAR knockdown can increase the sensitivity of NSCLC cells to radiation and cisplatin. The CCK‐8 results showed that cell viability was significantly increased in the overexpression group after radiation and cisplatin treatments. The overexpression group also showed more colonies, less apoptosis and DNA damage, and G2/M phase arrest was aggravated to provide the time necessary for DNA repair. Contrary to PANDAR overexpression, the trends were reversed in the PANDAR knockdown group. Furthermore, PANDAR knockdown inhibited radiation and cisplatin‐activated phosphorylation levels of ATR and CHK1 in NSCLC cells. Finally, our in vivo model showed that targeting PANDAR significantly sensitized NSCLC to radiation and cisplatin.
Conclusion
Our study showed that PANDAR knockdown promoted sensitivity to radiation and cisplatin in NSCLC by regulating the ATR/CHK1 pathway, thus providing a novel understanding as well as a therapeutic target for NSCLC treatment.
In NSCLC cells, lncRNA PANDAR negatively regulates sensitivity to radiation and cisplatin. PANDAR can promote the repair of radiation and cisplatin‐induced DNA damage and activation of the G2/M checkpoint through the ATR/CHK1 pathway. PANDAR knockdown results in defects in DNA damage repair accompanied by more cell apoptosis.
In non‐small cell lung cancer (NSCLC) cells, lncRNA PANDAR negatively regulates sensitivity to radiation and cisplatin. PANDAR can promote the repair of radiation and cisplatin‐induced DNA damage and activation of the G2/M checkpoint through the ATR/CHK1 pathway. PANDAR knockdown results in defects in DNA damage repair accompanied by more cell apoptosis.</abstract><cop>England</cop><pub>Wiley Periodicals Inc</pub><pmid>37460393</pmid><doi>10.1002/jgm.3565</doi><tpages>10</tpages></addata></record> |
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| subjects | Animals Antisense DNA Antisense RNA Apoptosis Apoptosis - genetics Ataxia Telangiectasia Mutated Proteins - genetics Ataxia Telangiectasia Mutated Proteins - metabolism Ataxia Telangiectasia Mutated Proteins - therapeutic use cancer Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - therapy Cell cycle Cell Line, Tumor Cell Proliferation - genetics Cell viability cell‐therapy Chemotherapy CHK1 protein Cholecystokinin Cisplatin Cisplatin - pharmacology Comet assay DNA Damage DNA repair DNA Repair - genetics Flow cytometry Humans Immunofluorescence lung Lung cancer Lung Neoplasms - drug therapy Lung Neoplasms - therapy Mice molecular‐genetics Non-coding RNA Non-small cell lung carcinoma Phosphorylation Radiation Ribonucleic acid RNA RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Small cell lung carcinoma Therapeutic targets tumor therapy |
| title | Long non‐coding RNA PANDAR promoted radiation and cisplatin‐induced DNA damage repair through ATR/CHK1 in NSCLC |
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