ArticleBritish journal of cancer2013
Role of endoplasmic reticulum stress induction by the plant toxin, persin, in overcoming resistance to the apoptotic effects of tamoxifen in human breast cancer cells.
Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Combination treatment with epibrassinolide overcomes tamoxifen resistance in breast cancer cells via endoplasmic reticulum stress induction.Molecular biology reports · 2025Article
- Oxeiptosis: a novel pathway of melanocytes death in response to oxidative stress in vitiligo.Cell death discovery · 2022Article
- Interactions Between Natural Products and Tamoxifen in Breast Cancer: A Comprehensive Literature Review.Frontiers in pharmacology · 2022Review
- Endocrine resistance in breast cancer: from molecular mechanisms to therapeutic strategies.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Aberrant fatty acid profile and FFAR4 signaling confer endocrine resistance in breast cancer.Journal of experimental & clinical cancer research : CR · 2019Article
- Kaempferol induces hepatocellular carcinoma cell death via endoplasmic reticulum stress-CHOP-autophagy signaling pathway.Oncotarget · 2017Article
- Microtubule-stabilizing properties of the avocado-derived toxins (+)-(R)-persin and (+)-(R)-tetrahydropersin in cancer cells and activity of related synthetic analogs.Investigational new drugs · 2016Article
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPersin is a plant toxin that displays synergistic cytotoxicity with tamoxifen in human breast cancer cell lines. Here, we examined the ability of persin to circumvent tamoxifen resistance and delineated the intracellular signalling pathways involved.
methodsThe induction of apoptosis in tamoxifen-resistant and -sensitive breast cancer cells was measured by flow cytometry following treatment with persin±tamoxifen. Markers of endoplasmic reticulum stress (ERS) were analysed following treatment, and their causal role in mediating persin-induced apoptosis was determined using chemical inhibitors and RNA interference.
resultsCells that were resistant to an apoptotic concentration of tamoxifen maintained an apoptotic response to persin. Persin-induced apoptosis was associated with an increase in markers of ERS, that is, CHOP expression and XBP-1 splicing and was decreased by CHOP siRNA. The CASP-4 inhibitor Z-YVAD-FMK markedly inhibited persin-induced apoptosis in both tamoxifen-sensitive and -resistant cells.
conclusionThe cytotoxic effects of persin are CASP-4 dependent and mediated by CHOP-dependent and -independent ERS signalling cascades. Increased ERS signalling contributes to persin-induced reversal of tamoxifen resistance.
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