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

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dc.contributor.authorJoo-Young Im-
dc.contributor.authorBo Kyung Kim-
dc.contributor.authorS H Yoon-
dc.contributor.authorB C Cho-
dc.contributor.authorY M Baek-
dc.contributor.authorMi-Jung Kang-
dc.contributor.authorN Kim-
dc.contributor.authorY D Gong-
dc.contributor.authorMi Sun Won-
dc.date.accessioned2021-05-11T03:30:27Z-
dc.date.available2021-05-11T03:30:27Z-
dc.date.issued2021-
dc.identifier.issn1226-3613-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/24323-
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.publisherSpringer-Nature Pub Group-
dc.titleDGG-100629 inhibits lung cancer growth by suppressing the NFATc1/DDIAS/STAT3 pathway-
dc.title.alternativeDGG-100629 inhibits lung cancer growth by suppressing the NFATc1/DDIAS/STAT3 pathway-
dc.typeArticle-
dc.citation.titleExperimental and Molecular Medicine-
dc.citation.number4-
dc.citation.endPage653-
dc.citation.startPage643-
dc.citation.volume53-
dc.contributor.affiliatedAuthorJoo-Young Im-
dc.contributor.affiliatedAuthorBo Kyung Kim-
dc.contributor.affiliatedAuthorMi-Jung Kang-
dc.contributor.affiliatedAuthorMi Sun Won-
dc.contributor.alternativeName임주영-
dc.contributor.alternativeName김보경-
dc.contributor.alternativeName윤성훈-
dc.contributor.alternativeName조병철-
dc.contributor.alternativeName백유미-
dc.contributor.alternativeName강미정-
dc.contributor.alternativeName김나연-
dc.contributor.alternativeName공영대-
dc.contributor.alternativeName원미선-
dc.identifier.bibliographicCitationExperimental and Molecular Medicine, vol. 53, no. 4, pp. 643-653-
dc.identifier.doi10.1038/s12276-021-00601-2-
dc.description.journalClassY-
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Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
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