Survive or die? c-MYC has the last word.

S Wu,X Liu,X Yin,L Chu

doi:10.1038/cddis.2015.366

Abstract

Survive or die? c-MYC has the last word.

Highlights

Metabolic alteration is one of the important characters in cancer cells, which confers advantages for survival and proliferation of cancer cells
We further found that glucose deprivation (GD) differentially affected c-MYC protein stability through affecting c-MYC phosphorylation in different cancer cell lines
We discovered that c-MYC was induced by GD in MDA-MB-231 cells

Summary

Introduction

Metabolic alteration is one of the important characters in cancer cells, which confers advantages for survival and proliferation of cancer cells. A lot of work demonstrated that metabolic change might be an adaption to tumor microenvironment and aberrant oncogene activation or tumor suppressor loss.[3] Most metabolic enzymes and regulators are the targets of oncogenes or tumor suppressor genes.[4] For example, oncogene c-MYC, which is deregulated in most of human cancers, was reported to drive the cancer cell metabolic reprogramming.[5] more and more data show that the interaction between metabolic alteration and tumor microenvironment or oncogene/tumor suppressor is mutual. C-MYC was previously demonstrated to promote both glucose metabolism and glutamine metabolism.[5] Recently, a Cell Death Discovery article by us showed that c-MYC was differentially affected by glucose deprivation (GD).[6] An interesting finding of our work is that GD decreases c-MYC protein levels in some cancer cell lines, but increases c-MYC in other cancer cell lines (Figure 1).

Results

Conclusion