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Arginine is an epigenetic regulator targeting TEAD4 to modulate OXPHOS in prostate cancer cells
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Arginine is an epigenetic regulator targeting TEAD4 to modulate OXPHOS in prostate cancer cells
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Journal Article
Arginine is an epigenetic regulator targeting TEAD4 to modulate OXPHOS in prostate cancer cells
2021
Overview
Arginine plays diverse roles in cellular physiology. As a semi-essential amino acid, arginine deprivation has been used to target cancers with arginine synthesis deficiency. Arginine-deprived cancer cells exhibit mitochondrial dysfunction, transcriptional reprogramming and eventual cell death. In this study, we show in prostate cancer cells that arginine acts as an epigenetic regulator to modulate histone acetylation, leading to global upregulation of nuclear-encoded oxidative phosphorylation (OXPHOS) genes. TEAD4 is retained in the nucleus by arginine, enhancing its recruitment to the promoter/enhancer regions of OXPHOS genes and mediating coordinated upregulation in a YAP1-independent but mTOR-dependent manner. Arginine also activates the expression of lysine acetyl-transferases and increases overall levels of acetylated histones and acetyl-CoA, facilitating TEAD4 recruitment. Silencing of TEAD4 suppresses OXPHOS functions and prostate cancer cell growth in vitro and in vivo. Given the strong correlation of TEAD4 expression and prostate carcinogenesis, targeting TEAD4 may be beneficially used to enhance arginine-deprivation therapy and prostate cancer therapy.
Alterations in metabolism and amino acid usage are common in cancer cells. Here, the authors show in prostate cancer cells that arginine globally upregulates nuclear-encoded oxidative phosphorylation genes by altering histone acetylation and retaining TEAD4 in the nucleus to transactivate genes.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 45/15
/ 45/23
/ 45/61
/ Animals
/ Arginine
/ DNA-Binding Proteins - genetics
/ DNA-Binding Proteins - metabolism
/ Epigenesis, Genetic - drug effects
/ Gene Expression Regulation, Neoplastic - drug effects
/ Genes
/ Histones
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ Lysine
/ Male
/ Mice
/ Muscle Proteins - metabolism
/ Oxidative Phosphorylation - drug effects
/ Prostatic Neoplasms - genetics
/ Prostatic Neoplasms - metabolism
/ Prostatic Neoplasms - pathology
/ Science
/ Signal Transduction - drug effects
/ Signal Transduction - genetics
/ TEA Domain Transcription Factors
/ Transcription Factors - genetics
