ArticleOncotarget2014
Caspase-8-mediated PAR-4 cleavage is required for TNFα-induced apoptosis.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- The Antitumor Potential of λ-Carrageenan Oligosaccharides on Gastric Carcinoma by Immunomodulation.Nutrients · 2023Article
- Structural Analysis of the cl-Par-4 Tumor Suppressor as a Function of Ionic Environment.Biomolecules · 2021Article
- Prostate apoptosis response-4 and tumor suppression: it's not just about apoptosis anymore.Cell death & disease · 2021Review
- PAR-4 overcomes chemo-resistance in breast cancer cells by antagonizing cIAP1.Scientific reports · 2019Article
- Review: Precision medicine and driver mutations: Computational methods, functional assays and conformational principles for interpreting cancer drivers.PLoS computational biology · 2019Review
- pH-Induced Folding of the Caspase-Cleaved Par-4 Tumor Suppressor: Evidence of Structure Outside of the Coiled Coil Domain.Biomolecules · 2018Article
- TNF-α and IFN-γ Together Up-Regulates Par-4 Expression and Induce Apoptosis in Human Neuroblastomas.Biomedicines · 2017Article
- ROS-induced cleavage of NHLRC2 by caspase-8 leads to apoptotic cell death in the HCT116 human colon cancer cell line.Cell death & disease · 2017Article
- A Naturally Generated Decoy of the Prostate Apoptosis Response-4 Protein Overcomes Therapy Resistance in Tumors.Cancer research · 2017Article
- A journey beyond apoptosis: new enigma of controlling metastasis by pro-apoptotic Par-4.Clinical & experimental metastasis · 2016Review
- The Role of Prostate Apoptosis Response-4 (Par-4) in Mycobacterium tuberculosis Infected Macrophages.Scientific reports · 2016Article
- Post-translational regulation of the cleaved fragment of Par-4 in ovarian and endometrial cancer cells.Oncotarget · 2016Article
- Chorein addiction in VPS13A overexpressing rhabdomyosarcoma cells.Oncotarget · 2015Article
- The structural basis for cancer treatment decisions.Oncotarget · 2014Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor protein prostate apoptosis response-4 (PAR-4) is silenced in a subset of human cancers and its down-regulation serves as a mechanism for cancer cell survival following chemotherapy. PAR-4 re-expression selectively causes apoptosis in cancer cells but how its pro-apoptotic functions are controlled and executed precisely is currently unknown. We demonstrate here that UV-induced apoptosis results in a rapid caspase-dependent PAR-4 cleavage at EEPD131G, a sequence that was preferentially recognized by caspase-8. To investigate the effect on cell growth for this cleavage event we established stable cell lines that express wild-type-PAR-4 or the caspase cleavage resistant mutant PAR-4 D131G under the control of a doxycycline-inducible promoter. Induction of the wild-type protein but not the mutant interfered with cell proliferation, predominantly through induction of apoptosis. We further demonstrate that TNFα-induced apoptosis leads to caspase-8-dependent PAR-4-cleavage followed by nuclear accumulation of the C-terminal PAR-4 (132-340) fragment, which then induces apoptosis. Taken together, our results indicate that the mechanism by which PAR-4 orchestrates the apoptotic process requires cleavage by caspase-8.
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