ArticlePLoS biology2025
Caspase 3 and caspase 7 promote cytoprotective autophagy and the DNA damage response during non-lethal stress conditions in human breast cancer cells.
Article in PLoS biology, 2025. 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.
- Epigallocatechin Gallate Modulates the Cellular Response to Doxorubicin in HeLa Cervical Cancer Cells.Biomolecules · 2026Article
- Berberine Modulates Mitophagy-Related Gene Expression and Suppresses Breast Cancer Cells: A Multi-Omics and Experimental Study.Cell biochemistry and biophysics · 2026Article
- Persistent loss of membrane-associated MUC4 reprograms physiological functions in corneal epithelial cells via MAPK-dependent cascade.Scientific reports · 2026Article
- Biocompatibility and Cell Death Mechanisms Induced by PMMA-Based Dental Materials in Gingival Fibroblasts and OECM-1 Tumor Cells.Dentistry journal · 2026Article
- Aneuploidy sensitizes cells to SREBP-pathway inhibition in squamous cell carcinoma.bioRxiv : the preprint server for biology · 2026Article
- Proton Irradiation Induces Differential Cellular Responses and Proteomic Signatures in Chondrosarcoma and Chondrocytes.Current issues in molecular biology · 2026Article
- RIP kinase inhibition with Necrostatin-1 improves human marginal mass islet graft survival and function for the management of type 1 diabetes.Cell death & disease · 2026Article
- Comparative Protective Effects of ATP and TPP Against Olaparib-Induced Ovarian Injury in Rats: Insights from Biochemical Parameters, Histopathology, and IRE1α, Cleaved Caspase-3, LC3B, and NF-κB p65 Double Immunofluorescence.Drug design, development and therapy · 2026Article
- Remodeling the tumor immune microenvironment: mechanisms of crosstalk between regulated cell death macrophages.Frontiers in immunology · 2026Review
- Aristolochic acid I accelerates lung adenocarcinoma progression coupled with the upregulation of core oncogenic networks: an integrated network toxicology and experimental study.Frontiers in pharmacology · 2026Article
- Quercetin Increases Expression of Membrane-TRAIL in Glioblastoma Cells Resulting in Apoptosis.Cancers · 2025Article
- Mechanistic insights into the effects of Tris-2-butoxyethyl phosphate on multiple cancers using network toxicology and molecular docking.Scientific reports · 2025Article
- CDCP1 promotes the malignant phenotypes of nasopharyngeal carcinoma via the Wnt/β-catenin signaling pathway.BMC biotechnology · 2025Article
- Polybrominated diphenyl ether profiles in adipose tissues of breast cancer patients and their carcinogenic potential investigation based on network toxicology and molecular docking.Frontiers in chemistry · 2025Article
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13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell stress adaptation plays a key role in normal development and in various diseases including cancer. Caspases are activated in response to cell stress, and growing evidence supports their function in non-apoptotic cellular processes. A role for effector caspases in promoting stress-induced cytoprotective autophagy was demonstrated in Drosophila, but has not been explored in the context of human cells. We found a functionally conserved role for effector caspase 3 (CASP3) and caspase 7 (CASP7) in promoting starvation or proteasome inhibition-induced cytoprotective autophagy in human breast cancer cells. The loss of CASP3 and CASP7 resulted in an increase in PARP1 cleavage, reduction in LC3B and ATG7 transcript levels, and a reduction in H2AX phosphorylation, consistent with a block in autophagy and DNA damage-induced stress response pathways. Surprisingly, in non-lethal cell stress conditions, CASP7 underwent non-canonical processing at two calpain cleavage sites flanking a PARP1 exosite, resulting in stable CASP7-p29/p30 fragments. Expression of CASP7-p29/p30 fragment(s) could rescue H2AX phosphorylation in the CASP3 and CASP7 double knockout background. Strikingly, yet consistent with these phenotypes, the loss of CASP3 and CASP7 exhibited synthetic lethality with BRCA1 loss. These findings support a role for human caspases in stress adaptation through PARP1 modulation and reveal new therapeutic avenues for investigation.
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