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Fig. 4 | Cell Communication and Signaling

Fig. 4

From: PRMT5 enhances tumorigenicity and glycolysis in pancreatic cancer via the FBW7/cMyc axis

Fig. 4

PRMT5 regulates cMyc at the posttranslational level a. Decreased PRMT5 expression resulted in a reduction in the cMyc protein level but had little impact on the HIF1α protein level. b. Knockdown of PRMT5 had a subtle impact on cMyc mRNA levels. c. We treated PRMT5-silenced pancreatic cancer cells with the proteasome inhibitor MG132 and measured the level of cMyc. The western blot analysis results demonstrated that MG132 treatment reversed the down-regulation of cMyc caused by PRMT5 knockdown, suggesting that PRMT5 regulates cMyc protein stability. d. PRMT5-silenced MIA PaCa-2 and SW1990 cells and the corresponding control cells were treated with CHX for the indicated durations, and the protein levels of cMyc were determined by western blotting. e. PRMT5 knockdown decreased the protein stability of cMyc in MIA PaCa-2 and SW1990 cells. f. In HPDE cells, overexpression of PRMT5 increased cMyc expression at the protein level, while the dominant-negative mutant of PRMT5 (PRMT5DN) had no such effect. g-h. Overexpressing PRMT5 in HPDE cells could stabilize cMyc, while PRMT5DN had no such effect

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