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. 2020 Mar 25;11(12):3588–3595. doi: 10.7150/jca.42338

Figure 3.

Figure 3

MYC is identified as a target of METTL3-mediated m6A modification in PCa. (A) Bioinformatics predicted the interaction between METTL3 protein and MYC RNA in homo sapiens (http://pridb.gdcb.iastate.edu/RPISeq/index.html). (B) The correlation between METTL3 and MYC using TCGA database (http://gepia.cancer-pku.cn/). (C) The expression of METTL3 and MYC was detected by IHC assays in clinical 84 PCa specimens. The percentage of staining gradations of METTL3 and MYC in clinical 84 PCa specimens was shown. (D) The correlation between METTL3 and MYC using IHC assays in clinical 84 PCa specimens. (E) The effect of METTL3 knockdown on the expression of MYC in C42 cells. (F) The effect of wild-type METTL3 and catalytic mutant METTL3 on the protein level of MYC in PC3 cells. (G) Gene-specific m6A qPCR validation of mRNA transcript level changes of MYC in C42 cells infected with NC or si-METTL3 and PC3 cells infected with Ctrl, METTL3-WT, or METTL3-MUT. (H-J) MYC over-expression rescued METTL3 knockdown-mediated inhibition of C42 cells proliferation (H), migration (I), invasion (J).