PRMT5 imposed a dual repression on DDIT3 transcription to promote the malignancy of hepatocellular carcinoma

Figure 5 DDIT3 restored the phenotype mediated by PRMT5 or HLCL-61. A and B: The protein levels of PRMT5 and DDIT3 were examined by western blot; C and D: DDIT3 rescued the growth of hepatocellular carcinoma (HCC) cells mediated by PRMT5; E and F: DDIT3 restored the clone formation of HCC cells mediated by PRMT5; G and H: Down-regulation of DDIT3 reduced the cell apoptosis of HCC cells induced by knocking down PRMT5 expression. Data are presented as the mean ± SD. ^aP < 0.05. ^bP < 0.01. ^cP < 0.001. NS: Not significant; Scr: Scramble; OD: Optical density; FITC: Fluorescein isothiocyanate; PI: Propidium iodide; shPRMT5: Short hairpin RNA of PRMT5; shDDIT3: Short hairpin RNA of DDIT3.