scholarly journals Induction of Estrogen Receptor β-mediated Autophagy Sensitizes Breast Cancer Cells to TAD1822-7, a Novel Biphenyl Urea Taspine Derivative

2021 ◽  
Author(s):  
Qi Su ◽  
Qing Wu ◽  
Kun Chen ◽  
Jingjing Wang ◽  
Ammar Sarwar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Annexin V ◽  
Female Breast Cancer ◽  
Estrogen Receptor Β ◽  
Inhibitory Effects ◽  
Insight Into

Abstract Female breast cancer has become the most commonly diagnosed cancer worldwide. As a tumor suppressor, estrogen receptor β (ERβ) is a potential target for breast cancer therapy. TAD1822-7 was evaluated for ERβ-mediated autophagy and cell death using cell proliferation assay, Annexin V/PI staining, immunofluorescence, western blotting and hypoxia cell models. TAD1822-7 upregulated ERβ causing cell death and induced mitochondrial dysfunction and autophagy companied with mitochondrial located ERβ. Enhanced levels of LC3-II and p62 indicated that TAD1822-7 blocked the late-stage autolysosome formation, leading to cell death. Mechanistically, TAD1822-7-induced cell death was mediated by PI3K/AKT signaling pathways. Moreover, TAD1822-7 modulated HIF functions and autophagy via the inhibition of HIF-1β in the context of hypoxia-induced autophagy. TAD1822-7 inhibited hypoxia-inducted autophagy and PI3K/AKT pathway. These findings provide new insight into the mechanism underlying the inhibitory effects of TAD1822-7 via ERβ-mediated pathways in breast cancer cells.

scholarly journals Agonists and knockdown of estrogen receptor β differentially affect invasion of triple-negative breast cancer cells in vitro

BMC Cancer ◽  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Susanne Schüler-Toprak ◽  
Julia Häring ◽  
Elisabeth C. Inwald ◽  
Christoph Moehle ◽  
Olaf Ortmann ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Estrogen Receptor Β

Knockdown of PTEN decreases expression of estrogen receptor β and tamoxifen sensitivity of human breast cancer cells

Steroids ◽  
2020 ◽  
Vol 153 ◽  
pp. 108521
Author(s):  
Oliver Treeck ◽  
Susanne Schüler-Toprak ◽  
Maciej Skrzypczak ◽  
Florian Weber ◽  
Olaf Ortmann
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Estrogen Receptor Β ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Tamoxifen Sensitivity

scholarly journals Cordyceps militaris Induces Immunogenic Cell Death and Enhances Antitumor Immunogenic Response in Breast Cancer

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Xingguo Quan ◽  
Beom Seok Kwak ◽  
Ji-Young Lee ◽  
Jin Hee Park ◽  
Anbok Lee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Checkpoint Inhibitors ◽  
Apoptotic Cell ◽  
Annexin V ◽  
Cfse Dilution ◽  
Mouse Breast Cancer ◽  
Treated Breast

Cordyceps militaris has been widely used as a traditional medicine in East Asia. Its effects against breast cancer have been reported previously. However, whether C. militaris-induced breast cancer cell death is immunogenic remains unelucidated. This study aimed to determine whether ethanolic extracts of C. militaris (CM-EE) could induce immunogenic cell death (ICD) in breast cancer immunotherapy to improve the efficacy of immune checkpoint inhibitors. Human and mouse breast cancer cells were treated with various concentrations of CM-EE for 72 h, and cytotoxicity was measured using the sulforhodamine B assay. Flow cytometry was used to assess cell death with annexin V/7-AAD staining and measure the surface exposure of damage-associated molecular pattern (DAMP) molecules including calreticulin, HSP70, and HSP90. Western blot for cleaved poly (ADP-ribose) polymerase (PARP) was used to confirm apoptotic cell death. The immunogenicity of CM-EE-induced dead cells was evaluated using the CFSE dilution assay. CM-EE reduced the viability of human (MCF7, MDA-MB-231, HS578T, and SKBR3) and mouse (4T1-neu-HA, TUBO-HA, and TUBO-P2J-HA) breast cancer cells. The IC50 was 25–50 µg/ml in human breast cancer cells and 10–50 µg/ml in mouse breast cancer cells at 72 h. CM-EE-treated breast cancer cells were positively stained by annexin V, cleaved PARP, and cleaved caspase 3/7 which were increased upon CM-EE treatment. Surface exposure of DAMP molecules was increased in dose- and time-dependent manners. The CFSE dilution assay revealed that dendritic cells fed with CM-EE-treated breast cancer cells successfully stimulated tumor-specific T cell proliferation without inhibiting DC function and T cell proliferation. The expression of PD-L1 mRNA and protein level was increased in dose-dependent manners. In addition, CM-EE also potentiated the cytotoxic activity of tumor-specific T cells. CM-EE can induce immunogenic and apoptotic cell death in breast cancer cells, and it is a good candidate for cancer immunotherapy and may improve the efficacy of immune checkpoint inhibitors.

scholarly journals Ginkgetin induces cell death in breast cancer cells via downregulation of the estrogen receptor

2017 ◽  
Vol 14 (4) ◽  
pp. 5027-5033 ◽  
Author(s):  
Yoonhwa Park ◽  
Sang Hyeok Woo ◽  
Sung-Keum Seo ◽  
Hyunggee Kim ◽  
Woo Chul Noh ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells
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