Copyright: ©Author(s) 2026.
World J Gastroenterol. May 21, 2026; 32(19): 115332
Published online May 21, 2026. doi: 10.3748/wjg.v32.i19.115332
Published online May 21, 2026. doi: 10.3748/wjg.v32.i19.115332
Figure 3 PRMT5 suppressed DDIT3 transcription by increasing H4R3me2 modification at the DDIT3 promoter.
A and B: The effect of PRMT5 overexpression and knockdown on DDIT3 promoter activity in hepatocellular carcinoma (HCC) cells; C: Location diagram of designed chromatin immunoprecipitation (ChIP) primers on DDIT3 promoter; D: ChIP examined the enrichment of PRMT5 on DDIT3 promoter; E and F: The level of H4R3me2 of DDIT3 promoter was evaluated in PRMT5 overexpression and knockdown HCC cells by ChIP assay. Data are presented as the mean ± SD. aP < 0.05. bP < 0.01. cP < 0.001. NS: Not significant; Scr: Scramble; IgG: Immunoglobulin G; shPRMT5: Short hairpin RNA of PRMT5.
- Citation: Jiang H, Yan JH, Tang WJ, Shen B, Mo S, Wang Y, Hu DH, Dong ZX, Zhang SB. PRMT5 imposed a dual repression on DDIT3 transcription to promote the malignancy of hepatocellular carcinoma. World J Gastroenterol 2026; 32(19): 115332
- URL: https://www.wjgnet.com/1007-9327/full/v32/i19/115332.htm
- DOI: https://dx.doi.org/10.3748/wjg.v32.i19.115332