The apple dihydrochalcone phloretin suppresses growth and improves chemosensitivity of breast cancer cells via inhibition of cytoprotective autophagy

2021 ◽  
Author(s):  
Ming Chen ◽  
Vemana Gowd ◽  
Mingfu Wang ◽  
Feng Chen ◽  
Ka-Wing Cheng
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Glucose Starvation ◽  
Starvation Stress ◽  
Schematic Representation

Schematic representation of the effect of phloretin-induced inhibition of cytoprotective autophagy in breast cancer cells under glucose starvation stress.

Glucose starvation greatly enhances antiproliferative and antiestrogenic potency of oligomycin A in MCF-7 breast cancer cells

Biochimie ◽  
2021 ◽  
Vol 186 ◽  
pp. 51-58
Author(s):  
Alexander M. Scherbakov ◽  
Danila V. Sorokin ◽  
Olga A. Omelchuk ◽  
Andrey E. Shchekotikhin ◽  
Mikhail A. Krasil’nikov
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Glucose Starvation ◽  
Oligomycin A ◽  
Mcf 7

scholarly journals Uev1A promotes breast cancer cell survival and chemoresistance through the AKT-FOXO1-BIM pathway

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Zhaojia Wu ◽  
Tong Niu ◽  
Wei Xiao
Keyword(s):  
Breast Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Akt Signaling ◽  
Serum Starvation ◽  
Starvation Stress ◽  
Starvation Conditions

Abstract Background Ubiquitin-conjugating enzyme variant UEV1A is required for Ubc13-catalyzed K63-linked poly-ubiquitination that regulates several signaling pathways including NF-κB, MAPK and PI3K/AKT. Previous reports implicate UEV1A as a potential proto-oncogene and have shown that UEV1A promotes breast cancer metastasis through constitutive NF-кB activation. Ubc13-Uev1A along with TARF6 can also ubiquitinate AKT but its downstream events are unclear. Methods In this study, we experimentally manipulated UEV1 expression in two typical breast cancer cell lines MDA-MB-231 and MCF7 under serum starvation conditions and monitored AKT activation and its downstream protein levels, as well as cellular sensitivity to chemotherapeutic agents. Results We found that overexpression of UEV1A is sufficient to activate the AKT signaling pathway that in turn inhibits FOXO1 and BIM expression to promote cell survival under serum starvation conditions and enhances cellular resistance to chemotherapy. Consistently, experimental depletion of Uev1 in breast cancer cells inhibits AKT signaling and promotes FOXO1 and BIM expression to reduce cell survival under serum starvation stress and enhance chemosensitivity. Conclusions Uev1A promotes cell survival under serum starvation stress through the AKT-FOXO1-BIM axis in breast cancer cells, which unveals a potential therapeutic target in the treatment of breast cancers.

scholarly journals Nm23-H1 activator phenylbutenoid dimer exerts cytotoxic effects on metastatic breast cancer cells by inducing mitochondrial dysfunction only under glucose starvation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bokyung Kim ◽  
Jae-Jin Lee ◽  
Ji Soo Shin ◽  
Ji-Wan Suh ◽  
Sunhee Jung ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Metastatic Breast ◽  
Atp Synthesis ◽  
Glucose Starvation ◽  
Cytotoxic Effects ◽  
Anti Cancer

AbstractMitochondrial oxidative phosphorylation (OXPHOS) has become an attractive target in anti-cancer studies in recent years. In this study, we found that a small molecule phenylbutenoid dimer NMac1 (Nm23-H1 activator 1), (±)-trans-3-(3,4-dimethoxyphenyl)-4-[(E)-3,4-dimethoxystyryl]cyclohex-1-ene, a previously identified anti-metastatic agent, has novel anti-proliferative effect only under glucose starvation in metastatic breast cancer cells. NMac1 causes significant activation of AMPK by decreasing ATP synthesis, lowers mitochondrial membrane potential (MMP, ΔΨm), and inhibits oxygen consumption rate (OCR) under glucose starvation. These effects of NMac1 are provoked by a consequence of OXPHOS complex I inhibition. Through the structure–activity relationship (SAR) study of NMac1 derivatives, NMac24 was identified as the most effective compound in anti-proliferation. NMac1 and NMac24 effectively suppress cancer cell proliferation in 3D-spheroid in vivo-like models only under glucose starvation. These results suggest that NMac1 and NMac24 have the potential as anti-cancer agents having cytotoxic effects selectively in glucose restricted cells.

scholarly journals KDM2A-dependent reduction of rRNA transcription on glucose starvation requires HP1 in cells, including triple-negative breast cancer cells

Oncotarget ◽  
2019 ◽  
Vol 10 (46) ◽  
pp. 4743-4760
Author(s):  
Kengo Okamoto ◽  
Yuji Tanaka ◽  
Sachiko Ogasawara ◽  
Chikashi Obuse ◽  
Jun-ichi Nakayama ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Glucose Starvation ◽  
Rrna Transcription ◽  
In Cells

The proliferation of breast cancer cells are inhibited by the human intrabody targeting cyclinD1

2010 ◽  
Vol 34 (8) ◽  
pp. S49-S49
Author(s):  
Lei Wang ◽  
Xun Zhou ◽  
Lihong Zhou ◽  
Yong Chen ◽  
Xun Zhu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells
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