Fig. 2: YTHDF1 promotes the cell cycle transition in PCa.

The knockdown of YTHDF1 in DU145 cells significantly decreased the incorporation efficiency of BrdU, with (B) presenting the statistical analysis of (A). Scale bar = 100 μm. C Statistic results for the FACS analysis of YTHDF1 knockdown leading to an increased number of cells in the G0/G1 phase. D Immunoblot analysis demonstrated the changes in the expression of cell cycle-related proteins, including CDK2, CDK4, CDK6, and p27, following YTHDF1 knockdown. The overexpression of YTHDF1 in RWPE-1 cells was assessed, with (E) analyzing mRNA levels and (F) analyzing protein levels. The green arrow indicates exogenous YTHDF1-flag, while the black arrow denotes endogenous YTHDF1. G The overexpression of YTHDF1 in RWPE-1 cells enhances tumor cell growth. The overexpression of YTHDF1 in RWPE-1 cells increases BrdU incorporation efficiency, with (I) representing the statistical analysis of (H). Scale bar = 100 μm. J, K Organoid images derived from prostatic Pten and Tp53 knockout mice (Pten^−/−; TP53^−/−), with or without mouse mYTHDF1 knockdown. The statistical result was presented in (K) for (J). Organoid images derived from prostatic Pten knockout mice (Pten^-/-), with or without YTHDF1 knockdown. The statistical result was presented in (M) for (L). N Images of xenograft tumors. O Silencing YTHDF1 resulted in reduced tumor volume. Immunohistochemical (IHC) analysis of xenograft tumors, including H&E staining and expressions of YTHDF1 and Ki67, with (Q) representing the statistical analysis of (P). YTH ove = YTHDF1 overexpression. Means ± SEM, *P < 0.05; **P < 0.01; ***P < 0.001; t-test.