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

Figure 1 PRMT5 predicted poor prognosis of hepatocellular carcinoma patients and inhibition of PRMT5 significantly reduced the viability of hepatocellular carcinoma cells. A and B: Using online database (GEPIA2) to analyze the overall survival and disease-free survival of hepatocellular carcinoma (HCC) patients with PRMT5 low and high expression; C and D: The protein levels of PRMT5 in stable cell lines were assessed by western blot, and the effect of PRMT5 on clone formation of HCC cells was examined by crystal violet assay; E and F: The growth of PRMT5 overexpression and knockdown HCC cells was detected by methylthiazolyldiphenyl-tetrazolium bromide assay; G: The cell viability of HCC cells treated with HLCL-61 at different concentration for 24 hours; H: The inhibition of HLCL-61 on growth of HCC cells with different malignancy at different concentration for 72 hours. Data are presented as the mean ± SD. ^bP < 0.01. ^cP < 0.001. VC: Vector; Scr: Scramble; PVTT: Portal vein tumor thrombus; OD: Optical density; shPRMT5: Short hairpin RNA of PRMT5.