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• W4289783575 abstract "Abstract N 6 -methyladenosine (m 6 A) modification is pivotal transcripts chemical modification of eukaryotic, which has been identified to play critical roles on tumor metabolic reprogramming. However, the functions of m 6 A reading protein YTH N 6 -methyladenosine RNA binding protein 3 (YTHDF3) in osteosarcoma is still unclear. This research planed to investigate the bio-functions and mechanism in osteosarcoma tumorigenesis. Results indicated that YTHDF3 up-regulated in the osteosarcoma tissue samples and cells, and closely correlated to the poor prognosis of osteosarcoma patients. Functionally, gain and loss-of-functional assays illustrated that YTHDF3 promoted the proliferation and aerobic glycolysis of osteosarcoma cells in vitro , and accelerated the tumor growth in vivo . Mechanistically, a m 6 A-modified PGK1 mRNA functioned as the target of YTHDF3, and YTHDF3 enhanced the PGK1 mRNA stability via m 6 A-dependent manner. In conclusion, these findings indicated that YTHDF3 functioned as an oncogene in osteosarcoma tumorigenesis through m 6 A/PGK1 manner, providing a therapeutic strategy for human osteosarcoma." @default.
• W4289783575 created "2022-08-04" @default.
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• W4289783575 date "2022-08-04" @default.
• W4289783575 modified "2023-10-16" @default.
• W4289783575 title "N6-methyladenosine reader YTHDF3 contributes to the aerobic glycolysis of osteosarcoma through stabilizing PGK1 stability" @default.
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• W4289783575 doi "https://doi.org/10.21203/rs.3.rs-1899379/v1" @default.
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