Fig. 3: USP39 exerts its pro-proliferative effect in a spliceosome-dependent manner. | Cell Death & Disease

Fig. 3: USP39 exerts its pro-proliferative effect in a spliceosome-dependent manner.

From: USP39 promotes hepatocellular carcinogenesis through regulating alternative splicing in cooperation with SRSF6/HNRNPC

Fig. 3: USP39 exerts its pro-proliferative effect in a spliceosome-dependent manner.The alternative text for this image may have been generated using AI.

A Flag-USP39 (WT) and Flag-USP39 (C139A) were introduced to USP39-deficiency (sh3) SNU-449 cells and verified with qRT-PCR and WB assays. B RIP experiments were performed using antibodies against Flag in the indicated cells. The levels of U1, U2, U4, and U6 snRNA in immunoprecipitated RNA were detected using qRT-PCR and normalized to the levels of U5 snRNA in each sample (n = 3). C CCK8 assay showed that only wild-type USP39, but not C139A mutant, could rescue the inhibition effect of USP39 deficiency on cell proliferation. D Representative images and quantification of foci formation induced by the indicated cells (n = 3). E Cells were synchronized at the G2/M boundary after being treated with thymidine and nocodazole. Following the release, the cells arrested in G2/M (0 h) would reenter the G1 phase (4 h). Cell cycle profiles showed changes in G1 cell populations at 4 h post-release. C139A mutant failed to rescue cell cycle arrest caused by USP39 knockdown (n = 3). Mean ± SD. P values by paired (B) or unpaired Student’s t-test (A, C–E). ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. ns: not significant.

Back to article page