Editing Nutrient sensing (section)

==Nutrient sensing and epigenetics==

Nutrient sensing and signaling is a key regulator of [[Epigenetics|epigenetic]] machinery in cancer. During glucose shortage, the energy sensor AMPK activates arginine methyltransferase [[CARM1]] and mediates [[histone H3]] hypermethylation ([[H3R17me2]]), leading to enhanced [[autophagy]]. In addition, [[Protein O-GlcNAc transferase|''O''-GlcNAc transferase (OGT)]] signals glucose availability to TET3 and inhibits TET3 by both decreasing its dioxygenase activity and promoting its nuclear export. OGT is also known to directly modify histones with [[O-GlcNAc|''O''-GlcNAc]]. These observations strongly suggest that nutrient signaling directly targets epigenetic enzymes to control epigenetic modifications.<ref>{{cite journal | vauthors = Wang YP, Lei QY | title = Metabolic recoding of epigenetics in cancer | journal = Cancer Commun (Lond) | volume = 38 | issue = 1 | pages = 1–8 | pmid = 29784032 | pmc = 5993135 | doi = 10.1186/s40880-018-0302-3 | year = 2018 | doi-access = free }}</ref>