Caveolin-1 inhibits breast cancer stem cells via c-Myc-mediated metabolic reprogramming.

Cell Death & Disease
Shengqi WangZhiyu Wang

Abstract

Breast cancer stem cells (BCSCs) are considered to be the root of breast cancer occurrence and progression. However, the characteristics and regulatory mechanisms of BCSCs metabolism have been poorly revealed, which hinders the development of metabolism-targeted treatment strategies for BCSCs elimination. Herein, we demonstrated that the downregulation of Caveolin-1 (Cav-1) usually occurred in BCSCs and was associated with a metabolic switch from mitochondrial respiration to aerobic glycolysis. Meanwhile, Cav-1 could inhibit the self-renewal capacity and aerobic glycolysis activity of BCSCs. Furthermore, Cav-1 loss was associated with accelerated mammary-ductal hyperplasia and mammary-tumor formation in transgenic mice, which was accompanied by enrichment and enhanced aerobic glycolysis activity of BCSCs. Mechanistically, Cav-1 could promote Von Hippel-Lindau (VHL)-mediated ubiquitination and degradation of c-Myc in BCSCs through the proteasome pathway. Notably, epithelial Cav-1 expression significantly correlated with a better overall survival and delayed onset age of breast cancer patients. Together, our work uncovers the characteristics and regulatory mechanisms of BCSCs metabolism and highlights Cav-1-targeted treatments as...Continue Reading

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Citations

Oct 3, 2020·Molecular Cancer·Tianshui SunQing Yang
Dec 12, 2020·Journal of Neurochemistry·Yizhen TangXinghuai Sun
Dec 4, 2020·International Journal of Molecular Sciences·Sara El-Sahli, Lisheng Wang
Jan 20, 2021·Clinical and Translational Medicine·Neng WangZhiyu Wang
Jan 30, 2021·Journal of Experimental & Clinical Cancer Research : CR·Youqin XuWenhua Huang
Sep 10, 2021·Journal of Cancer Research and Clinical Oncology·Xingning LaiLixia Xiong

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Methods Mentioned

BETA
transgenic
xenograft
transfection
flow cytometry
ubiquitination
Immunoprecipitation
xenografts
Transmission

Software Mentioned

SPSS

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