DC Field | Value | Language |
---|---|---|
dc.contributor.author | Joo-Young Im | - |
dc.contributor.author | Bo Kyung Kim | - |
dc.contributor.author | Ji Young Lee | - |
dc.contributor.author | Seung Ho Park | - |
dc.contributor.author | Hyun Seung Ban | - |
dc.contributor.author | K E Jung | - |
dc.contributor.author | Mi Sun Won | - |
dc.date.accessioned | 2018-04-19T05:19:10Z | - |
dc.date.available | 2018-04-19T05:19:10Z | - |
dc.date.issued | 2018 | - |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.uri | 10.1038/s41388-017-0025-y | ko |
dc.identifier.uri | https://oak.kribb.re.kr/handle/201005/17777 | - |
dc.description.abstract | DNA damage-induced apoptosis suppressor (DDIAS) has an anti-apoptotic function during DNA damage in lung cancer. However, the anti-apoptotic mechanism of DDIAS in cancer cells under other conditions has not been reported. We report here that DDIAS protects cancer cells from tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by two distinct mechanisms in non-small cell lung cancer (NSCLC) and hepatocellular carcinoma (HCC) cells. DDIAS depletion sensitized NSCLC and HCC cells to TRAIL-mediated apoptosis, an effect that was abrogated by pharmacological or genetic inhibition of caspase-8 and was independent of caspase-9, p53, or mitogen-activated protein kinase signaling. Interestingly, we found that the N terminus of DDIAS interacted with the death effector domain of Fas-associated protein death domain (FADD) and prevented its recruitment to the death-inducing signaling complex (DISC), thereby blocking caspase-8 activation. DDIAS knockdown also suppressed epidermal growth factor-induced phosphorylation of p90 ribosomal S6 kinase (RSK) 2 and stabilized caspase-8 by preventing its ubiquitination and proteasomal degradation. This effect was abolished by RSK2 overexpression. Taken together, DDIAS has dual functions in inhibiting DISC formation as well as in destabilizing caspase-8, thereby suppressing TRAIL-mediated apoptosis of cancer cells. Thus, we suggest that DDIAS can serve as an effective therapeutic target in the treatment of NSCLC and HCC | - |
dc.publisher | Springer-Nature Pub Group | - |
dc.title | DDIAS suppresses TRAIL-mediated apoptosis by inhibiting DISC formation and destabilizing caspase-8 in cancer cells | - |
dc.title.alternative | DDIAS suppresses TRAIL-mediated apoptosis by inhibiting DISC formation and destabilizing caspase-8 in cancer cells | - |
dc.type | Article | - |
dc.citation.title | Oncogene | - |
dc.citation.number | 0 | - |
dc.citation.endPage | 1262 | - |
dc.citation.startPage | 1251 | - |
dc.citation.volume | 37 | - |
dc.contributor.affiliatedAuthor | Joo-Young Im | - |
dc.contributor.affiliatedAuthor | Bo Kyung Kim | - |
dc.contributor.affiliatedAuthor | Ji Young Lee | - |
dc.contributor.affiliatedAuthor | Seung Ho Park | - |
dc.contributor.affiliatedAuthor | Hyun Seung Ban | - |
dc.contributor.affiliatedAuthor | Mi Sun Won | - |
dc.contributor.alternativeName | 임주영 | - |
dc.contributor.alternativeName | 김보경 | - |
dc.contributor.alternativeName | 이지영 | - |
dc.contributor.alternativeName | 박승호 | - |
dc.contributor.alternativeName | 반현승 | - |
dc.contributor.alternativeName | 정경은 | - |
dc.contributor.alternativeName | 원미선 | - |
dc.identifier.bibliographicCitation | Oncogene, vol. 37, pp. 1251-1262 | - |
dc.identifier.doi | 10.1038/s41388-017-0025-y | - |
dc.description.journalClass | Y | - |
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