Mitochondrial biogenesis drives tumor cell proliferation.

摘要

Little is known about the mechanism(s) of arsenic-induced carcinogenesis. A study published by Lee et al in this issue of The American Journal of Pathology directly addressed this through study of arsenic-induced Bow-en's disease and demonstration of increased mitochon-drial biogenesis as a crucial determinant of carcinogenesis. In this study, keratinocyte exposure to low-dose arsenic leads to mitochondrial biogenesis and increased proliferation. Pharmacological or genetic down-regulation of mitochondrial biogenesis abrogates this growth advantage.