NAT10 mediated ac4C acetylation driven m⁶A modification via involvement of YTHDC1-LDHA/PFKM regulates glycolysis and promotes osteosarcoma.

ABSTRACT: The dynamic changes of RNA N6-methyladenosine (m⁶A) during cancer progression participate in various cellular processes. However, less is known about a possible direct connection between upstream regulator and m⁶A modification, and therefore affects oncogenic progression. Here, we have identified that a key enzyme in N4-acetylcytidine (ac4C) acetylation NAT10 is highly expressed in human osteosarcoma tissues, and its knockdown enhanced m⁶A contents and significantly suppressed osteosarcoma cell growth, migration and invasion. Further results revealed that NAT10 silence inhibits mRNA stability and translation of m⁶A reader protein YTHDC1, and displayed an increase in glucose uptake, a decrease in lactate production and pyruvate content. YTHDC1 rec

SUBMITTER: Mei Z 

PROVIDER: S-EPMC10795323 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature