ArticleOncogene2003
Paclitaxel-induced apoptosis in BJAB cells proceeds via a death receptor-independent, caspases-3/-8-driven mitochondrial amplification loop.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
68 citing papers in PubMed, 177 citations in OpenAlex.
- Mechanisms of Paclitaxel Resistance: Recent Advances and Future Perspectives.International journal of molecular sciences · 2026Review
- The Role of Caspases in Melanoma Pathogenesis.Current issues in molecular biology · 2024Review
- In-vivo studies of targeted and localized cancer drug release from microporous poly-di-methyl-siloxane (PDMS) devices for the treatment of triple negative breast cancer.Scientific reports · 2024Article
- Article
- Paclitaxel promotes mTOR signaling-mediated apoptosis in esophageal cancer cells by targeting MUC20.Thoracic cancer · 2023Article
- Fungal 7-epi-10-deacetyltaxol produced by an endophytic Pestalotiopsis microspora induces apoptosis in human hepatocellular carcinoma cell line (HepG2).BMC complementary and alternative medicine · 2017Article
- Bax/Bak-independent mitochondrial depolarization and reactive oxygen species induction by sorafenib overcome resistance to apoptosis in renal cell carcinoma.The Journal of biological chemistry · 2017Article
- Apoptosis resistance, mitotic catastrophe, and loss of ploidy control in Burkitt lymphoma.Journal of molecular medicine (Berlin, Germany) · 2015Article
- The role of individual caspases in cell death induction by taxanes in breast cancer cells.Cancer cell international · 2015Article
- Induction of apoptosis and necroptosis by 24(S)-hydroxycholesterol is dependent on activity of acyl-CoA:cholesterol acyltransferase 1.Cell death & disease · 2014Article
- Ultrasound-mediated destruction of LHRHa-targeted and paclitaxel-loaded lipid microbubbles induces proliferation inhibition and apoptosis in ovarian cancer cells.Molecular pharmaceutics · 2014Article
- Arrestins in apoptosis.Handbook of experimental pharmacology · 2014Article
- Caspase-cleaved arrestin-2 and BID cooperatively facilitate cytochrome C release and cell death.Cell death and differentiation · 2014Article
- Inhibition of cathepsin B by E-64 induces oxidative stress and apoptosis in filarial parasite.PloS one · 2014Article
- Inhibition of cancer cell proliferation and apoptosis-inducing activity of fungal taxol and its precursor baccatin III purified from endophytic Fusarium solani.Cancer cell international · 2013Article
- Targeted therapy of the XIAP/proteasome pathway overcomes TRAIL-resistance in carcinoma by switching apoptosis signaling to a Bax/Bak-independent 'type I' mode.Cell death & disease · 2013Article
- Caspase-2 is involved in cell death induction by taxanes in breast cancer cells.Cancer cell international · 2013Article
- The caspase pathway of linoelaidic acid (9t, 12t-c18:2)-induced apoptosis in human umbilical vein endothelial cells.Lipids · 2013Article
- A DR4:tBID axis drives the p53 apoptotic response by promoting oligomerization of poised BAX.The EMBO journal · 2012Article
- Identification of Simple Compounds with Microtubule-Binding Activity That Inhibit Cancer Cell Growth with High Potency.ACS medicinal chemistry letters · 2012Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caspase-8 is a key effector of death-receptor-triggered apoptosis. In a previous study, we demonstrated, however, that caspase-8 can also be activated in a death receptor-independent manner via the mitochondrial apoptosis pathway, downstream of caspase-3. Here, we show that caspases-3 and -8 mediate a mitochondrial amplification loop that is required for the optimal release of cytochrome c, mitochondrial permeability shift transition, and cell death during apoptosis induced by treatment with the microtubule-damaging agent paclitaxel (Taxol). In contrast, Smac release from mitochondria followed a different pattern, and therefore seems to be regulated independently from cytochrome c release. Taxol-induced cell death was inhibited by the use of synthetic, cell-permeable caspase-3- (zDEVD-fmk) or caspase-8-specific (zIETD-fmk) inhibitors. Apoptosis signaling was not affected by a dominant-negative FADD mutant (FADD-DN), thereby excluding a role of death receptor signaling in the amplification loop and drug-induced apoptosis. The inhibitor experiments were corroborated by the use of BJAB cells overexpressing the natural serpin protease inhibitor, cytokine response modifier A. These data demonstrate that the complete activation of mitochondria, release of cytochrome c, and execution of drug-induced apoptosis require a mitochondrial amplification loop that depends on caspases-3 and -8 activation. In addition, this is the first report to demonstrate death receptor-independent caspase-8 autoprocessing in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.