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- W315031804 abstract "The newly identified tumor suppressor, N-myc downstream-regulated gene 2 (NDRG2), has been studied in various cancers because of its anticancer and antimetastasis effects. In this study, we examined the effect of NDRG2 expression on cell viability in MDA-MB-231 human breast cancer cells under conditions that are similar to the microenvironment of solid tumors, which include glucose deprivation. NDRG2 overexpression enhanced the pro-apoptotic effects of glucose deprivation. Glucose deprivation also induced the activation of AMP-activated protein kinase (AMPK), which plays a role in protecting tumor cells from metabolic stresses. NDRG2 overexpression strongly reduced glucose deprivation-induced AMPK phosphorylation and increased the cleavage of poly (ADP-ribose) polymerase (PARP), which indicated the induction of apoptosis. The expression of a constitutively active form of AMPK effectively blocked glucose deprivation-induced apoptosis in NDRG2-overexpressing MDA-MB-231 cells. Moreover, NDRG2 overexpression also enhanced the pro-apoptotic effects of 2-deoxyglucose (2-DG) or hypoxia, an inducer of metabolic stresses. Finally, we showed that LKB1 is an upstream kinase of AMPK that is involved in the inhibition of glucose deprivation-induced AMPK activity in NDRG2-overexpressing cells. Our findings collectively suggest that NDRG2 is a negative regulator of AMPK activity and functions as a sensitizer of glucose deprivation." @default.
- W315031804 created "2016-06-24" @default.
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- W315031804 date "2014-06-26" @default.
- W315031804 modified "2023-10-12" @default.
- W315031804 title "NDRG2 overexpression enhances glucose deprivation-mediated apoptosis in breast cancer cells via inhibition of the LKB1-AMPK pathway" @default.
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- W315031804 doi "https://doi.org/10.18632/genesandcancer.17" @default.
- W315031804 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4104758" @default.
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