We are analyzing https://link.springer.com/article/10.1186/bcr2602.

Title:
Tamoxifen enhances the cytotoxic effects of nelfinavir in breast cancer cells | Breast Cancer Research
Description:
Introduction The HIV protease inhibitor nelfinavir is currently under investigation as a new anti-cancer drug. Several studies have shown that nelfinavir induces cell cycle arrest, endoplasmic reticulum stress, autophagy, and apoptosis in cancer cells. In the present article, the effect of nelfinavir on human breast cancer cells is examined and potential combination treatments are investigated. Methods The effects of nelfinavir and tamoxifen on the human breast cancer cell lines MCF7, T47 D, MDA-MB-453, and MDA-MB-435 were tested by analysing their influence on cell viability (via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay), apoptosis (annexin binding, poly(ADP-ribose) polymerase cleavage), autophagy (autophagy marker light chain 3B expression), endoplasmic reticulum stress (binding protein and activating transcription factor 3 expression), and the occurrence of oxidative stress (intracellular glutathione level). Results Nelfinavir induced apoptosis in all four breast cancer cell lines tested, although the extent of autophagy and endoplasmic reticulum stress varied among the cell lines. The concentration of nelfinavir needed for an efficient induction of apoptosis in breast cancer cells could be reduced from 15 μg/ml to 6 μg/ml when combined with tamoxifen. At a concentration of 6 μg/ml, tamoxifen substantially enhanced the endoplasmic reticulum stress reaction in those cell lines that responded to nelfinavir with binding protein (BiP) upregulation (MCF7, T47D), and enhanced autophagy in cell lines that responded to nelfinavir treatment with autophagy marker light chain 3B upregulation (MDA-MB-453). Although tamoxifen has been described to be able to induce oxidative stress at concentrations similar to those applied in this study (6 μg/ml), we observed that nelfinavir but not tamoxifen reduced the intracellular glutathione level of breast cancer cells within hours of application by up to 32%, suggesting the induction of oxidative stress was an early event and an additional cause of the apoptosis induced by nelfinavir. Conclusions The results demonstrate that nelfinavir may be an effective drug against breast cancer and could be combined with tamoxifen to enhance its efficacy against breast cancer cells. Moreover, the cytotoxic effect of a tamoxifen and nelfinavir combination was independent of the oestrogen receptor status of the analysed breast cancer cells, suggesting a potential benefit of a combination of these two drugs even in patients with no hormone-responsive tumours. We therefore recommend that clinical studies on nelfinavir with breast cancer patients should include this drug combination to analyse the therapeutic efficacy as well as the safety and tolerability of this potential treatment option.
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nelfinavir, cells, cancer, cell, breast, tamoxifen, article, figure, pubmed, google, scholar, stress, mdamb, glutathione, cas, μgml, combination, apoptosis, mcf, endoplasmic, effect, lines, reticulum, concentrations, effects, akt, treatment, observed, autophagy, oestrogen, drugs, activity, protein, hours, analysed, levels, protease, assay, culture, germany, incubated, hiv, inhibitor, drug, reduced, death, authors, intracellular, proteasome, analysis,

Topics {✒️}

extracellular signal-regulated kinase endoplasmic reticulum-induced stress stress-induced cell damage perk/eif2α/atf4 module chromogenic bcip/nbt assay hormone receptor-independent effects 5-diphenyl-2h-tetrazolium bromide signaling regulator grp78/bip trypan blue-excluding cells full size image article download pdf tamoxifen-induced adduct formation pleiotropic anti-cancer effects oestrogen receptor-negative erk1/2-mediated mcl-1 stabilization alkaline phosphatase-coupled antibodies cell survival-related proteins ludwig-maximilians-university munich lower lc3b-ii band cell-protective mechanism oestrogen receptor-positive hormone receptor status german research foundation mda-mb-435 cells survived klaus friese & alexander burges cell signaling technology cell cycle retardation synergistic anti-tumour effects anti-apoptotic mcl-1 protein alkaline phosphatase detection sorafenib-mediated mcl-1 downregulation endoplasmic reticulum stress breast cancer patients bioluminescent proteasome assay node-negative patients akt-1 mediates survival full access hiv protease inhibitors mek1/erk pathways 5 mm n-acetyl-cysteine oestrogen receptor status cell lines respond hiv protease inhibitor hiv-infected persons breast cancer cells related subjects pi3k/akt pathway inhibition potential negative interaction nelfinavir-treated mda-mb-453 privacy choices/manage cookies

Questions {❓}

Chow WA, Jiang C, Guan M: Anti-HIV drugs for cancer therapeutics: back to the future?

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         headline:Tamoxifen enhances the cytotoxic effects of nelfinavir in breast cancer cells
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