We are analyzing https://link.springer.com/article/10.1007/s10549-011-1364-y.

Title:
Addition of a histone deacetylase inhibitor redirects tamoxifen-treated breast cancer cells into apoptosis, which is opposed by the induction of autophagy | Breast Cancer Research and Treatment
Description:
Modulation of estrogen signaling is one of the most successful modalities for the treatment of estrogen receptor (ER)-positive breast cancer, yet de novo and acquired resistance are frequent. Recent data suggests that the induction of autophagy may play a considerable role in promoting tumor cell survival and resistance to anti-estrogen therapy. Hence, bypassing autophagy may offer a novel strategy to enhance the anti-tumor efficacy of anti-estrogens. Histone deacetylases (HDAC) are involved in the regulation of steroid hormone receptor mediated cell signaling and their inhibition potentiates the anti-tumor effects of anti-estrogens. However, the mechanism underlying this anti-tumor activity is poorly understood. In this report, we show that the addition of an HDAC inhibitor redirects the response of ER-positive breast cancer cells when treated with tamoxifen from growth arrest to apoptotic cell death. This redirection requires functional ER signaling and is mediated by a depletion of Bcl-2 and an induction of Bax and Bak, manifesting in cytochrome C release and PARP cleavage. With combined treatment, a subpopulation of cells is refractory to apoptosis and exhibit a strong induction of autophagy. Inhibition of autophagy in these cells, using siRNA directed against Beclin-1 or treatment with chloroquine, further promotes the induction of apoptosis. Thus, supporting prior reports that autophagy acts as a survival mechanism, our findings demonstrate that HDAC and autophagy inhibition directs autophagy-protected cells into apoptotic cell death, which may impair development of tamoxifen resistance.
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Keywords {🔍}

article, cancer, pubmed, google, scholar, cas, breast, cells, autophagy, histone, deacetylase, cell, apoptosis, hdac, inhibition, death, treatment, inhibitor, estrogen, receptor, res, induction, resistance, human, expression, research, tamoxifen, access, privacy, cookies, content, antiestrogen, therapy, treat, clin, data, publish, search, thomas, signaling, role, tumor, antiestrogens, mechanism, refractory, oncol, lymphoma, information, log, journal,

Topics {✒️}

month download article/chapter cutaneous t-cell lymphoma 4-hydroxytamoxifen-induced cell death blocks tamoxifen-induced proliferation breast cancer cells estrogen receptor alpha positive breast cancer human breast cancer hdac inhibitor redirects functional estrogen receptor suberoylanilide hydroxamic acid anti-estrogen therapy therapeutic drug group histone deacetylase enhances human breast dcis full article pdf phase ii trial histone deacetylase inhibition human gastric cancer malignant glioma cells tumor suppressor mechanism privacy choices/manage cookies tamoxifen-induced killing related subjects histone h4 acetylation apoptotic cell death myc-induced model anti-tumor efficacy anti-tumor effects enhances mitochondrial depolarization anti-estrogens tamoxifen 10 μm 4oh-tamoxifen anti-proliferative action estrogen receptor anti-tumor activity estrogen signaling article thomas lung cancer patients check access instant access european economic area supporting prior reports mitochondrial membrane permeabilization double-edged sword electronic supplementary material dye exclusion assay histone deacetylase 1 histone deacetylase 2 histone deacetylase-1 recent data suggests

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         description:Modulation of estrogen signaling is one of the most successful modalities for the treatment of estrogen receptor (ER)-positive breast cancer, yet de novo and acquired resistance are frequent. Recent data suggests that the induction of autophagy may play a considerable role in promoting tumor cell survival and resistance to anti-estrogen therapy. Hence, bypassing autophagy may offer a novel strategy to enhance the anti-tumor efficacy of anti-estrogens. Histone deacetylases (HDAC) are involved in the regulation of steroid hormone receptor mediated cell signaling and their inhibition potentiates the anti-tumor effects of anti-estrogens. However, the mechanism underlying this anti-tumor activity is poorly understood. In this report, we show that the addition of an HDAC inhibitor redirects the response of ER-positive breast cancer cells when treated with tamoxifen from growth arrest to apoptotic cell death. This redirection requires functional ER signaling and is mediated by a depletion of Bcl-2 and an induction of Bax and Bak, manifesting in cytochrome C release and PARP cleavage. With combined treatment, a subpopulation of cells is refractory to apoptosis and exhibit a strong induction of autophagy. Inhibition of autophagy in these cells, using siRNA directed against Beclin-1 or treatment with chloroquine, further promotes the induction of apoptosis. Thus, supporting prior reports that autophagy acts as a survival mechanism, our findings demonstrate that HDAC and autophagy inhibition directs autophagy-protected cells into apoptotic cell death, which may impair development of tamoxifen resistance.
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