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SOD2 acetylation on lysine 68 promotes stem cell reprogramming in breast cancer
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SOD2 acetylation on lysine 68 promotes stem cell reprogramming in breast cancer
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Journal Article
SOD2 acetylation on lysine 68 promotes stem cell reprogramming in breast cancer
2019
Overview
Mitochondrial superoxide dismutase (SOD2) suppresses tumor initiation but promotes invasion and dissemination of tumor cells at later stages of the disease. The mechanism of this functional switch remains poorly defined. Our results indicate that as SOD2 expression increases acetylation of lysine 68 ensues. Acetylated SOD2 promotes hypoxic signaling via increased mitochondrial reactive oxygen species (mtROS). mtROS, in turn, stabilize hypoxia-induced factor 2α (HIF2α), a transcription factor upstream of “stemness” genes such as Oct4, Sox2, and Nanog. In this sense, our findings indicate that SOD2K68Ac and mtROS are linked to stemness reprogramming in breast cancer cells via HIF2α signaling. Based on these findings we propose that, as tumors evolve, the accumulation of SOD2K68Ac turns on a mitochondrial pathway to stemness that depends on HIF2α andmay be relevant for the progression of breast cancer toward poor outcomes.
Publisher
National Academy of Sciences
Subject
/ Animals
/ Basic Helix-Loop-Helix Transcription Factors - physiology
/ Breast Neoplasms - metabolism
/ Breast Neoplasms - pathology
/ Cell Self Renewal - physiology
/ Female
/ Humans
/ Hydrogen Peroxide - metabolism
/ Hypoxia
/ Lysine
/ Mice
/ Neoplasm Proteins - chemistry
/ Neoplasm Proteins - physiology
/ Neoplastic Stem Cells - physiology
/ Protein Processing, Post-Translational
/ Recombinant Proteins - metabolism
/ Superoxide Dismutase - chemistry
/ Superoxide Dismutase - physiology
/ Tumors
