We are analyzing https://link.springer.com/article/10.1007/s10549-007-9873-4.

Title:
Macroautophagy inhibition sensitizes tamoxifen-resistant breast cancer cells and enhances mitochondrial depolarization | Breast Cancer Research and Treatment
Description:
Macroautophagy (autophagy), a process for lysosomal degradation of organelles and long-lived proteins, has been linked to various pathologies including cancer and to the cellular response to anticancer therapies. In the human estrogen receptor positive MCF7 breast adenocarcinoma cell line, treatment with the endocrine therapeutic tamoxifen was shown previously to induce cell cycle arrest, cell death, and autophagy. To investigate specifically the role of autophagy in tamoxifen treated breast cancer cell lines, we used a siRNA approach, targeting three different autophagy genes, Atg5, Beclin-1, and Atg7. We found that knockdown of autophagy, in combination with tamoxifen in MCF7 cells, results in decreased cell viability concomitant with increased mitochondrial-mediated apoptosis. The combination of autophagy knockdown and tamoxifen treatment similarly resulted in reduced cell viability in the breast cancer cell lines, estrogen receptor positive T-47D and tamoxifen-resistant MCF7-HER2. Together, these results indicate that autophagy has a primary pro-survival role following tamoxifen treatment, and suggest that autophagy knockdown may be useful in a combination therapy setting to sensitize breast cancer cells, including tamoxifen-resistant breast cancer cells, to tamoxifen therapy.
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Keywords {🔍}

article, pubmed, google, scholar, cas, cancer, autophagy, cell, breast, cells, death, tamoxifen, apoptosis, biol, research, treatment, estrogen, receptor, kondo, content, human, role, resistance, res, inhibition, access, nat, mol, differ, privacy, cookies, macroautophagy, tamoxifenresistant, mcf, atg, therapy, clin, publish, search, mitochondrial, response, positive, endocrine, lines, beclin, factor, protein, growth, regulation, klionsky,

Topics {✒️}

her2/pi-3k/akt activation leads er/her2-positive breast cancer tamoxifen-resistant mcf7-her2 month download article/chapter tamoxifen-resistant tumorigenic growth increased mitochondrial-mediated apoptosis breast cancer cells estrogen receptor-positive gonzalez-polo ra org/docroot/home/index macroautophagy triggers apoptosis abbott research grant enhances mitochondrial depolarization tamoxifen-induced apoptosis malignant glioma cells yeast autophagy-related genes mcf7 cells mcf-7 cells transfected primary pro-survival role full article pdf calpain-mediated cleavage pathologies including cancer privacy choices/manage cookies growth factor regulation myc-induced model radiation-induced autophagy breast cancer autophagy-related becn1 endocrine therapeutic tamoxifen related subjects activating transcription factor-2 autophagic cell death atg7-beclin 1 program cancer cells gfp-lc3 plasmid anti-estrogens tamoxifen reduced cell viability cell cycle control high content screening check access instant access lysosomotropic agent monodansylcadaverine apoptosis/autophagy paradox her2/neu european economic area long-lived proteins sirna approach agonist/antagonist activity double-edged sword dunn wa jr

Questions {❓}

Baehrecke EH (2005) Autophagy: dual roles in life and death?
Levine B, Yuan J (2005) Autophagy in cell death: an innocent convict?
Melino G, Knight RA, Nicotera P (2005) How many ways to die?

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         description:Macroautophagy (autophagy), a process for lysosomal degradation of organelles and long-lived proteins, has been linked to various pathologies including cancer and to the cellular response to anticancer therapies. In the human estrogen receptor positive MCF7 breast adenocarcinoma cell line, treatment with the endocrine therapeutic tamoxifen was shown previously to induce cell cycle arrest, cell death, and autophagy. To investigate specifically the role of autophagy in tamoxifen treated breast cancer cell lines, we used a siRNA approach, targeting three different autophagy genes, Atg5, Beclin-1, and Atg7. We found that knockdown of autophagy, in combination with tamoxifen in MCF7 cells, results in decreased cell viability concomitant with increased mitochondrial-mediated apoptosis. The combination of autophagy knockdown and tamoxifen treatment similarly resulted in reduced cell viability in the breast cancer cell lines, estrogen receptor positive T-47D and tamoxifen-resistant MCF7-HER2. Together, these results indicate that autophagy has a primary pro-survival role following tamoxifen treatment, and suggest that autophagy knockdown may be useful in a combination therapy setting to sensitize breast cancer cells, including tamoxifen-resistant breast cancer cells, to tamoxifen therapy.
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      headline:Macroautophagy inhibition sensitizes tamoxifen-resistant breast cancer cells and enhances mitochondrial depolarization
      description:Macroautophagy (autophagy), a process for lysosomal degradation of organelles and long-lived proteins, has been linked to various pathologies including cancer and to the cellular response to anticancer therapies. In the human estrogen receptor positive MCF7 breast adenocarcinoma cell line, treatment with the endocrine therapeutic tamoxifen was shown previously to induce cell cycle arrest, cell death, and autophagy. To investigate specifically the role of autophagy in tamoxifen treated breast cancer cell lines, we used a siRNA approach, targeting three different autophagy genes, Atg5, Beclin-1, and Atg7. We found that knockdown of autophagy, in combination with tamoxifen in MCF7 cells, results in decreased cell viability concomitant with increased mitochondrial-mediated apoptosis. The combination of autophagy knockdown and tamoxifen treatment similarly resulted in reduced cell viability in the breast cancer cell lines, estrogen receptor positive T-47D and tamoxifen-resistant MCF7-HER2. Together, these results indicate that autophagy has a primary pro-survival role following tamoxifen treatment, and suggest that autophagy knockdown may be useful in a combination therapy setting to sensitize breast cancer cells, including tamoxifen-resistant breast cancer cells, to tamoxifen therapy.
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