title: Epigenetic and metabolic regulation of breast cancer stem cells.
abstract: Breast cancer has a relatively high mortality rate in women due to recurrence and metastasis. Increasing evidence has identified a rare population of cells with stem cell-like properties in breast cancer. These cells, termed cancer stem cells (CSCs), which have the capacity for self-renewal and differentiation, contribute significantly to tumor progression, recurrence, drug resistance and metastasis. Clarifying the mechanisms regulating breast CSCs has important implications for our understanding of breast cancer progression and therapeutics. A strong connection has been found between breast CSCs and epithelial mesenchymal transition (EMT). In addition, recent studies suggest that the maintenance of the breast CSC phenotype is associated with epigenetic and metabolic regulation. In this review, we focus on recent discoveries about the connection between EMT and CSC, and advances made in understanding the roles and mechanisms of epigenetic and metabolic reprogramming in controlling breast CSC properties.
authors.affiliation: Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou 310058, China.
authors.forename: Hui-xin
authors.initials: HX
authors.lastname: Liu
authors.forename: Xiao-li
authors.initials: XL
authors.lastname: Li
authors.forename: Chen-fang
authors.initials: CF
authors.lastname: Dong
mesh_terms: D000818:Animals; D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism*; D002454:Cell Differentiation; D018450:Disease Progression; D019008:Drug Resistance, Neoplasm; D044127:Epigenesis, Genetic; D058750:Epithelial-Mesenchymal Transition; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008325:Mammary Neoplasms, Experimental / Q000378:metabolism; D051379:Mice; D009362:Neoplasm Metastasis; D009364:Neoplasm Recurrence, Local; D014411:Neoplastic Stem Cells / Q000166:cytology*; D010641:Phenotype
keywords: Breast cancer; Cancer stem cells (CSCs); Epigenetic modification; Epithelial mesenchymal transition (EMT); Metabolic reprogramming