ArticleOncogene2018
DDIAS suppresses TRAIL-mediated apoptosis by inhibiting DISC formation and destabilizing caspase-8 in cancer cells.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Molecular switches in cell death: the interplay of apoptosis and pyroptosis in cancer.Cell communication and signaling : CCS · 2026Review
- Pan-cancer analysis reveals DDIAS as a potential diagnostic biomarker, prognostic indicator, and tumor-immune correlate.Discover oncology · 2026Article
- ApoBDs: a paradigm shift from cellular debris to therapeutic vehicles.Frontiers in endocrinology · 2025Review
- Article
- Targeting caspase-8: a new strategy for combating hepatocellular carcinoma.Frontiers in immunology · 2024Review
- DDIAS, DNA damage-induced apoptosis suppressor, is a potential therapeutic target in cancer.Experimental & molecular medicine · 2023Review
- Expression of DR4, DR5, FAS, Caspase-8 and, DDIAS Genes in AML Patients.Medical journal of the Islamic Republic of Iran · 2023Article
- PSPC1 is a potential prognostic marker for hormone-dependent breast cancer patients and modulates RNA processing of ESR1 and SCFD2.Scientific reports · 2022Article
- Article
- DGG-100629 inhibits lung cancer growth by suppressing the NFATc1/DDIAS/STAT3 pathway.Experimental & molecular medicine · 2021Article
- Identification of cancer stem cell-related biomarkers in intestinal-type and diffuse-type gastric cancer by stemness index and weighted correlation network analysis.Journal of translational medicine · 2020Article
- RSK2 protects human breast cancer cells under endoplasmic reticulum stress through activating AMPKα2-mediated autophagy.Oncogene · 2020Article
- Miconazole inhibits signal transducer and activator of transcription 3 signaling by preventing its interaction with DNA damage-induced apoptosis suppressor.Cancer science · 2020Article
- DDIAS promotes STAT3 activation by preventing STAT3 recruitment to PTPRM in lung cancer cells.Oncogenesis · 2020Article
- Development and validation of a CIMP-associated prognostic model for hepatocellular carcinoma.EBioMedicine · 2019Article
- Network Pharmacology-Based Study on the Mechanism of Bushen-Jianpi Decoction in Liver Cancer Treatment.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Article
- Synthesis and biological evaluation of novel asymmetric naphthalene diimide derivatives as anticancer agents depending on ROS generation.MedChemComm · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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