May 8, 2021 · Downregulated FTO expression substantially increases the m 6 A modifications on MYC, resulting in the binding of YTHDF1 to promote MYC mRNA translation and tumor cell glycolysis and growth.

May 8, 2021 · Our findings uncovered a critical mechanism of epitranscriptome regulation by Wnt/β-catenin-mediated FTO downregulation and underscored the role of m 6 A modifications of MYC mRNA in regulating tumor cell glycolysis and growth.

The biological function of fat mass and obesity-associated protein (FTO) was determined in vivo and in vitro. The target genes of FTO were screened by MeRIP-seq, RT-qPCR and Western blot. The m6A binding proteins of target genes were verified by RNA pulldown and RNA immunoprecipitation assays.

Jan 11, 2018 · High levels of FTO sensitize leukemic cells to R-2HG, whereas hyperactivation of MYC signaling confers resistance that can be reversed by the inhibition of MYC signaling. R-2HG also displays anti-tumor activity in glioma.

Moreover, MYC activated by EBV in EBVaGC elevated FTO expression by binding to a specific region of the FTO promoter. Mechanistically, our work uncovered a crucial suppressive role of FTO in EBVaGC metastasis and invasiveness via an m6A‐FOS‐IGF2BP1/2‐dependent manner, suggesting a promising biomarker panel for GC metastatic prediction and therapy.

High levels of FTO sensitize leukemic cells to R-2HG, whereas hyperactivation of MYC signaling confers resistance that can be reversed by the inhibition of MYC signaling. R-2HG also displays anti-tumor activity in glioma.

Jun 1, 2021 · Here, we have identified the m6A demethylase FTO as an essential epitranscriptomic regulator utilized by tumors to escape immune surveillance through regulation of glycolytic metabolism.

Downregulated FTO expression substantially enhances the m6A levels in the mRNAs of a large number of genes in critical pathways, particularly metabolic pathway genes, such as MYC.

Jul 13, 2020 · These key observations uncover the tumor-initiating activities of HDAC3 in GC through its regulation on FOXA2-mediated FTO/m6A/MYC axis, highlighting the potential of therapeutically...

FTO improved the stability of PD-L1 mRNA in an m6A-dependent manner, and MYC promoted PD-L1 transcription. TAAs and FB23-2 co-delivered to TIDCs were expected to help ICBs inhibit HCC progression by increasing m6A methylation, enhancing T-cell infiltration, and generating immune memory.