Survival of cancer stem-like cells under metabolic stress via CaMK2 α-mediated upregulation of sarco/endoplasmic reticulum calcium ATPase expression.

CONCLUSIONS: The current study provides compelling evidence that CaMK2α acts as a key anti-apoptosis regulator in metabolic stress-resistant CSCs by activating NFκB. The latter induces expression of SERCA, allowing survival in glucose-deprived conditions. Importantly, our combination therapeutic strategy provides a novel approach for the clinical application of CSC treatment. PMID: 29279319 [PubMed - as supplied by publisher]

https://www.ncbi.nlm.nih.gov/pubmed/29279319?dopt=Abstract

Source: Clinical Cancer Research - December 26, 2017 Category: Cancer & Oncology Authors: Park KC, Kim SW, Jeon JY, Jo AR, Choi HJ, Kim JM, Lee HG, Kim Y, Mills GB, Noh SH, Lee MG, Park ES, Cheong JH Tags: Clin Cancer Res Source Type: research