100 87

Cited 0 times in

DGG-100629 inhibits lung cancer growth by suppressing the NFATc1/DDIAS/STAT3 pathway

DC Field Value Language
dc.contributor.author조병철-
dc.date.accessioned2021-09-29T02:25:41Z-
dc.date.available2021-09-29T02:25:41Z-
dc.date.issued2021-04-
dc.identifier.issn1226-3613-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/184886-
dc.description.abstractDNA damage-induced apoptosis suppressor (DDIAS) promotes the progression of lung cancer and hepatocellular carcinoma through the regulation of multiple pathways. We screened a chemical library for anticancer agent(s) capable of inhibiting DDIAS transcription. DGG-100629 was found to suppress lung cancer cell growth through the inhibition of DDIAS expression. DGG-100629 induced c-Jun NH(2)-terminal kinase (JNK) activation and inhibited NFATc1 nuclear translocation. Treatment with SP600125 (a JNK inhibitor) or knockdown of JNK1 restored DDIAS expression and reversed DGG-100629-induced cell death. In addition, DGG-100629 suppressed the signal transducer and activator of transcription (STAT3) signaling pathway. DDIAS or STAT3 overexpression restored lung cancer cell growth in the presence of DGG-100629. In a xenograft assay, DGG-100629 inhibited tumor growth by reducing the level of phosphorylated STAT3 and the expression of STAT3 target genes. Moreover, DGG-100629 inhibited the growth of lung cancer patient-derived gefitinib-resistant cells expressing NFATc1 and DDIAS. Our findings emphasize the potential of DDIAS blockade as a therapeutic approach and suggest a novel strategy for the treatment of gefitinib-resistant lung cancer.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherNature Publishing Group-
dc.relation.isPartOfEXPERIMENTAL AND MOLECULAR MEDICINE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleDGG-100629 inhibits lung cancer growth by suppressing the NFATc1/DDIAS/STAT3 pathway-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학교실)-
dc.contributor.googleauthorJoo-Young Im-
dc.contributor.googleauthorBo-Kyung Kim-
dc.contributor.googleauthorSung-Hoon Yoon-
dc.contributor.googleauthorByoung Chul Cho-
dc.contributor.googleauthorYu Mi Baek-
dc.contributor.googleauthorMi-Jung Kang-
dc.contributor.googleauthorNayeon Kim-
dc.contributor.googleauthorYoung-Dae Gong-
dc.contributor.googleauthorMisun Won-
dc.identifier.doi10.1038/s12276-021-00601-2-
dc.contributor.localIdA03822-
dc.relation.journalcodeJ00860-
dc.identifier.eissn2092-6413-
dc.identifier.pmid33859351-
dc.contributor.alternativeNameCho, Byoung Chul-
dc.contributor.affiliatedAuthor조병철-
dc.citation.volume53-
dc.citation.number4-
dc.citation.startPage643-
dc.citation.endPage653-
dc.identifier.bibliographicCitationEXPERIMENTAL AND MOLECULAR MEDICINE, Vol.53(4) : 643-653, 2021-04-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.