DC Field | Value | Language |
---|---|---|
dc.contributor.author | Joo-Young Im | - |
dc.contributor.author | Bo Kyung Kim | - |
dc.contributor.author | S H Yoon | - |
dc.contributor.author | B C Cho | - |
dc.contributor.author | Y M Baek | - |
dc.contributor.author | Mi-Jung Kang | - |
dc.contributor.author | N Kim | - |
dc.contributor.author | Y D Gong | - |
dc.contributor.author | Mi Sun Won | - |
dc.date.accessioned | 2021-05-11T03:30:27Z | - |
dc.date.available | 2021-05-11T03:30:27Z | - |
dc.date.issued | 2021 | - |
dc.identifier.issn | 1226-3613 | - |
dc.identifier.uri | https://oak.kribb.re.kr/handle/201005/24323 | - |
dc.description.abstract | DNA 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.publisher | Springer-Nature Pub Group | - |
dc.title | DGG-100629 inhibits lung cancer growth by suppressing the NFATc1/DDIAS/STAT3 pathway | - |
dc.title.alternative | DGG-100629 inhibits lung cancer growth by suppressing the NFATc1/DDIAS/STAT3 pathway | - |
dc.type | Article | - |
dc.citation.title | Experimental and Molecular Medicine | - |
dc.citation.number | 4 | - |
dc.citation.endPage | 653 | - |
dc.citation.startPage | 643 | - |
dc.citation.volume | 53 | - |
dc.contributor.affiliatedAuthor | Joo-Young Im | - |
dc.contributor.affiliatedAuthor | Bo Kyung Kim | - |
dc.contributor.affiliatedAuthor | Mi-Jung Kang | - |
dc.contributor.affiliatedAuthor | Mi Sun Won | - |
dc.contributor.alternativeName | 임주영 | - |
dc.contributor.alternativeName | 김보경 | - |
dc.contributor.alternativeName | 윤성훈 | - |
dc.contributor.alternativeName | 조병철 | - |
dc.contributor.alternativeName | 백유미 | - |
dc.contributor.alternativeName | 강미정 | - |
dc.contributor.alternativeName | 김나연 | - |
dc.contributor.alternativeName | 공영대 | - |
dc.contributor.alternativeName | 원미선 | - |
dc.identifier.bibliographicCitation | Experimental and Molecular Medicine, vol. 53, no. 4, pp. 643-653 | - |
dc.identifier.doi | 10.1038/s12276-021-00601-2 | - |
dc.description.journalClass | Y | - |
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