ArticleCell death & disease2017
Stability of the cancer target DDIAS is regulated by the CHIP/HSP70 pathway in lung cancer cells.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- NFATc1 activates the Ras/Raf/p38 MAPK pathway to promote the progression of lung adenocarcinoma.Translational cancer research · 2025Article
- CHIP/STUB1 suppresses the transcription and latent reactivation of HIV-1 via the TRAF6-NF-κB-HIV-LTR axis.PLoS pathogens · 2025Article
- Deciphering the tumour microenvironment of clear cell renal cell carcinoma: Prognostic insights from programmed death genes using machine learning.Journal of cellular and molecular medicine · 2024Article
- DNA Damage-Induced Apoptosis Suppressor Triggers Progression and Stemness of Glioma by Enhancing Lymphoid Enhancer-Binding Factor 1 Expression.World journal of oncology · 2024Article
- 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
- Chaperone-assisted E3 ligase CHIP: A double agent in cancer.Genes & diseases · 2022Review
- DGG-100629 inhibits lung cancer growth by suppressing the NFATc1/DDIAS/STAT3 pathway.Experimental & molecular medicine · 2021Article
- Extracellular signal regulated kinase 5 promotes cell migration, invasion and lung metastasis in a FAK-dependent manner.Protein & cell · 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
- CHIP-mediated ubiquitination of Galectin-1 predicts colorectal cancer prognosis.International journal of biological sciences · 2020Article
- Hsp90B enhances MAST1-mediated cisplatin resistance by protecting MAST1 from proteosomal degradation.The Journal of clinical investigation · 2019Article
- Development and validation of a CIMP-associated prognostic model for hepatocellular carcinoma.EBioMedicine · 2019Article
- Benzidine Induces Epithelial-Mesenchymal Transition of Human Bladder Cancer Cells through Activation of ERK5 Pathway.Molecules and cells · 2018Article
- DDIAS suppresses TRAIL-mediated apoptosis by inhibiting DISC formation and destabilizing caspase-8 in cancer cells.Oncogene · 2018Article
- CHIPped balance of proteostasis and longevity.Oncotarget · 2017Article
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) rescues lung cancer cells from apoptosis in response to DNA damage. DDIAS is transcriptionally activated by NFATc1 and EGF-mediated ERK5/MEF2B, leading to cisplatin resistance and cell invasion. Therefore, DDIAS is suggested as a therapeutic target for lung cancer. Here, we report that DDIAS stability is regulated by E3 U-box ubiquitin ligase carboxyl terminus of HSP70-interacting protein (CHIP)-mediated proteasomal degradation. We first isolated CHIP as an interacting partner of DDIAS by yeast two-hybrid screening. CHIP physically associated with both the N- and C-terminal regions of DDIAS, targeting it for proteasomal degradation and reducing the DDIAS half-life. CHIP overexpression analyses indicated that the tetratrico peptide repeat (TPR) domain and the U-box are required for DDIAS ubiquitination. It is likely that HSP70-bound DDIAS is recruited to the CHIP E3 ligase via the TPR domain, suggesting DDIAS as a client protein of HSP70. In addition, CHIP overexpression in lung cancer cells expressing high DDIAS levels induced significant growth inhibition by enhancing DDIAS degradation. Furthermore, simultaneous CHIP overexpression and DNA damage agent treatment caused a substantial increase in the apoptosis of lung cancer cells. Taken together, these findings indicate that the stability of the DDIAS protein is regulated by CHIP/HSP70-mediated proteasomal degradation and that CHIP overexpression stimulates the apoptosis of lung cancer cells in response to DNA-damaging agents.
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