ArticleCell death & disease2024
Caspase-3 promotes oncogene-induced malignant transformation via EndoG-dependent Src-STAT3 phosphorylation.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Evasion of cell death despite mitochondrial outer membrane permeabilization: an oncogenic outcome of apoptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Sublethal Caspase-8 Activation Drives Radiation-Induced Genetic Instability and Oncogenic Transformation Through Endonuclease G and Non-Canonical NF-κB Signaling.International journal of molecular sciences · 2026Article
- Article
- Hid and reaper differentially regulate apoptotic and non-apoptotic executioner caspase activation to control organ size.Cellular and molecular life sciences : CMLS · 2026Article
- Niclosamide attenuates skin cancer progression through suppression of key oncogenic pathways: integrated in vivo and in-silico mechanistic insights.BMC cancer · 2026Article
- Anti-cancer effects of carvacrol on NUF2, CASP3 and CLDN6 expression in T47D breast cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Caspase-3/7 deficiency results in enhanced intestinal inflammation and reduced tumorigenesis.Science advances · 2026Article
- Dying cells as architects of the stem cell niche: a conserved mechanism driving tissue regeneration and tumor therapy resistance.Cell communication and signaling : CCS · 2026Review
- Article
- Optimized detection of caspase-6 activation in a murine inflammation model to inform neurodegenerative disease therapies.PloS one · 2026Article
- Aberrant expression of nuclear prothymosin α contributes to epithelial-mesenchymal transition in lung cancer.Molecular oncology · 2025Article
- Mechanistic insights into the effects of Tris-2-butoxyethyl phosphate on multiple cancers using network toxicology and molecular docking.Scientific reports · 2025Article
- Sublethal executioner caspase activation in hepatocytes promotes liver regeneration through the JAK/STAT3 pathway.PLoS biology · 2025Article
- Nuclear-Localized BCKDK Facilitates Homologous Recombination Repair to Support Breast Cancer Progression and Therapy Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Efficacy of Pyrotinib combined with Trastuzumab in the treatment of patients with human epidermal growth factor receptor-2 positive breast cancer.Pakistan journal of medical sciences · 2025Article
- Specific signaling pathways mediated programmed cell death in tumor microenvironment and target therapies.Discover oncology · 2025Review
- Ferroptosis in Cancer: Mechanism and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Ebselen Alleviates Sepsis-Induced Acute Kidney Injury by Regulating Endoplasmic Reticulum Stress, Apoptosis, and Oxidative Stress.Veterinary medicine and science · 2025Article
- NGR1 reduces neuronal apoptosis through regulation of ITGA11 following subarachnoid hemorrhage.Molecular medicine reports · 2025Article
- Noncoding RNA-encoded peptides in cancer: biological functions, posttranslational modifications and therapeutic potential.Journal of hematology & oncology · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Accumulating evidence suggests that caspase-3 plays critical roles beyond apoptosis, serving pro-survival functions in malignant transformation and tumorigenesis. However, the mechanism of non-apoptotic action of caspase-3 in oncogenic transformation remains unclear. In the present study, we show that caspase-3 is consistently activated in malignant transformation induced by exogenous expression of oncogenic cocktail (c-Myc, p53DD, Oct-4, and H-Ras) in vitro as well as in the mouse mammary tumor virus-polyomavirus middle T antigen (MMTV-PyMT) mouse model of breast cancer. Genetic ablation of caspase-3 significantly attenuated oncogene-induced transformation of mammalian cells and delayed breast cancer progression in MMTV-PyMT transgenic mice. Mechanistically, active caspase-3 triggers the translocation of endonuclease G (EndoG) from mitochondria, which migrates to the nucleus, thereby induces phosphorylation of Src-STAT3 signaling pathway to facilitate oncogenic transformation. Taken together, our data suggest that caspase-3 plays pivotal role in facilitating rather than suppressing oncogene-induced malignant transformation of mammalian cells.
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