Cited 20 times in
Insulin-like growth factor-1 attenuates cisplatin-induced gammaH2AX formation and DNA double-strand breaks repair pathway in non-small cell lung cancer
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김세규 | - |
dc.contributor.author | 김형중 | - |
dc.date.accessioned | 2015-05-19T17:13:53Z | - |
dc.date.available | 2015-05-19T17:13:53Z | - |
dc.date.issued | 2008 | - |
dc.identifier.issn | 0304-3835 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/107752 | - |
dc.description.abstract | Because insulin-like growth factor-1 (IGF-1) counteracts the anti-neoplastic effect of cisplatin that induces DNA damage and cell death through the formation of platinum-DNA adducts, we investigated the effects of IGF-1 on the DNA double-strand breaks (DSBs) repair system induced by cisplatin. NCI-H1299 and H460 non-small cell lung cancer (NSCLC) cells treated with IGF-1 recovered from cisplatin-derived inhibited proliferation and apoptosis. Decreased tail length in comet assay and suppressed phosphorylation of histone H2AX at Ser139 with IGF-1 cotreatment indicates that IGF-1 attenuates cisplatin-induced DNA damage. Cotreatment with IGF-1 attenuates phosphorylation of ataxia-telangiectasia mutated (ATM) at Ser1981, and ATM-Rad3-related (ATR) at Ser428 and subsequent phosphorylation of Chk2, Chk1, and p53 also dwindled by IGF-1. On the other hand, suppression of the IGF system with AG1024 or siRNA of insulin receptor substrate-1 (IRS-1), a major adaptor molecule of the IGF system, augmented cisplatin-induced gammaH2AX, Ser1981-pATM, and Ser428-pATR generation. ATM, which plays an important role in the phosphorylation of histone H2AX and Chk2 at Thr68, strongly binds with IRS-1 under the influence of cisplatin, and the interaction was partially inhibited by IGF-1. Immunocytochemistry revealed that cisplatin induces nuclear translocation of IRS-1 with Ser1981-pATM, which is suppressed by cotreatment with IGF-1. In conclusion, cisplatin-induced gammaH2AX formation, DNA DSBs repair, and damage checkpoint pathway is inhibited by IGF-1. Cisplatin derives interaction between ATM and IRS-1, which is suppressed by IGF-1. Modulation of biologic activity of the IGF-1 system could be a promising modality that raises the response rate of conventional chemotherapy. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 232~241 | - |
dc.relation.isPartOf | CANCER LETTERS | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Antineoplastic Agents/pharmacology* | - |
dc.subject.MESH | Apoptosis | - |
dc.subject.MESH | Base Sequence | - |
dc.subject.MESH | Blotting, Western | - |
dc.subject.MESH | Carcinoma, Non-Small-Cell Lung/genetics | - |
dc.subject.MESH | Carcinoma, Non-Small-Cell Lung/metabolism* | - |
dc.subject.MESH | Carcinoma, Non-Small-Cell Lung/pathology | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | Cisplatin/pharmacology* | - |
dc.subject.MESH | Comet Assay | - |
dc.subject.MESH | DNA Damage* | - |
dc.subject.MESH | DNA Repair* | - |
dc.subject.MESH | Histones/biosynthesis* | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Immunohistochemistry | - |
dc.subject.MESH | Insulin-Like Growth Factor I/physiology* | - |
dc.subject.MESH | Lung Neoplasms/genetics | - |
dc.subject.MESH | Lung Neoplasms/metabolism* | - |
dc.subject.MESH | Lung Neoplasms/pathology | - |
dc.subject.MESH | RNA, Small Interfering | - |
dc.title | Insulin-like growth factor-1 attenuates cisplatin-induced gammaH2AX formation and DNA double-strand breaks repair pathway in non-small cell lung cancer | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Internal Medicine (내과학) | - |
dc.contributor.googleauthor | Jeong Hee Jeon | - |
dc.contributor.googleauthor | Se Kyu Kim | - |
dc.contributor.googleauthor | Hyung Jung Kim | - |
dc.contributor.googleauthor | Joon Chang | - |
dc.contributor.googleauthor | Chul Min Ahn | - |
dc.contributor.googleauthor | Yoon Soo Chang | - |
dc.identifier.doi | 10.1016/j.canlet.2008.07.011 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A00602 | - |
dc.contributor.localId | A01158 | - |
dc.relation.journalcode | J00448 | - |
dc.identifier.eissn | 1872-7980 | - |
dc.identifier.pmid | 18762365 | - |
dc.identifier.url | http://www.sciencedirect.com/science/article/pii/S0304383508005545 | - |
dc.subject.keyword | Non-small cell lung cancer | - |
dc.subject.keyword | Cisplatin | - |
dc.subject.keyword | Insulin-like growth factor-1 | - |
dc.subject.keyword | DNA DSBs repair system | - |
dc.subject.keyword | Damaged-DNA checkpoint | - |
dc.subject.keyword | Ataxia-telangiectasia mutated | - |
dc.subject.keyword | ATM-Rad3-related | - |
dc.subject.keyword | DNA-dependent protein kinase | - |
dc.subject.keyword | γH2AX | - |
dc.contributor.alternativeName | Kim, Se Kyu | - |
dc.contributor.alternativeName | Kim, Hyung Jung | - |
dc.contributor.affiliatedAuthor | Kim, Se Kyu | - |
dc.contributor.affiliatedAuthor | Kim, Hyung Jung | - |
dc.rights.accessRights | not free | - |
dc.citation.volume | 272 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 232 | - |
dc.citation.endPage | 241 | - |
dc.identifier.bibliographicCitation | CANCER LETTERS, Vol.272(2) : 232-241, 2008 | - |
dc.identifier.rimsid | 55306 | - |
dc.type.rims | ART | - |
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