Chaube , B. and Malvi, P. and Singh, S.V. and Mohammad , N. and Violeet , B. and Bhat , M.K. (2015) AMPK maintains energy homeostasis and survival in cancer cells via regulating p38/PGC-1α-mediated mitochondrial biogenesis. Cell Death and Discovery, 1. 15063-5063.

Text 68.Dr. Bhat M.K.(Cell Death & Discovery) paid open access .pdf Download (1949Kb)

Abstract

Cancer cells exhibit unique metabolic response and adaptation to the fluctuating microenvironment, yet molecular and biochemical events imprinting this phenomenon are unclear. Here, we show that metabolic homeostasis and adaptation to metabolic stress in cancer cells are primarily achieved by an integrated response exerted by the activation of AMPK. We provide evidence that AMPK-p38-PGC-1α axis, by regulating energy homeostasis, maintains survival in cancer cells under glucose-limiting conditions. Functioning as a molecular switch, AMPK promotes glycolysis by activating PFK2, and facilitates mitochondrial metabolism of non-glucose carbon sources thereby maintaining cellular ATP level. Interestingly, we noted that AMPK can promote oxidative metabolism via increasing mitochondrial biogenesis and OXPHOS capacity via regulating expression of PGC-1α through p38MAPK activation. Taken together, our study signifies the fundamental role of AMPK in controlling cellular bioenergetics and mitochondrial biogenesis in cancer cells.

Item Type:	Article
Additional Information:	This is open access articles for full text click above web link.
Subjects:	Cancer Biology
Depositing User:	Mr. Rameshwar Nema
Date Deposited:	22 Dec 2015 05:23
Last Modified:	19 Feb 2016 04:59
URI:	http://nccs.sciencecentral.in/id/eprint/221

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