Fig. 5

YTHDF1 facilitated the proliferation of HCC cells by activating PI3K/AKT/mTOR signaling pathway. A The results of GSEA indicated that PI3K/AKT/mTOR signaling pathway was enriched in HCC with YTHDF1-overexpression. B The correlation analysis between YTHDF1 and key molecules of PI3K/AKT/mTOR signaling pathway in HCC was performed by using GEPIA. C Western blot was performed to detect the protein levels of AKT, p-AKT, mTOR, p-mTOR in Huh7 and MHCC-97H cells with YTHDF1 knockdown. D Western blot was performed to detect the protein levels of AKT1, AKT2, and AKT3 in MHCC-97H cells with YTHDF1 silencing. E q-RT PCR was performed to measure the mRNA levels of AKT1, AKT2, and AKT3 in Huh7 and MHCC-97H cells with YTHDF1 silencing. F YTHDF1-deficient MHCC-97H cells treated with 4ug/ml SC79 for 1 h, cell proliferation was measured by Edu assay. Representative images and quantitative histograms were shown. *P < 0.05, **P < 0.01