Fig. 5: USP39 exerts its malignant effects partially through an isoform switch of KANK2-S to KANK2-L. | Cell Death & Disease

Fig. 5: USP39 exerts its malignant effects partially through an isoform switch of KANK2-S to KANK2-L.

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

Fig. 5: USP39 exerts its malignant effects partially through an isoform switch of KANK2-S to KANK2-L.The alternative text for this image may have been generated using AI.

A The mRNA level of USP39 and the expression proportion of KANK2-L isoform were detected in our in-house HCC cohort (n = 66). B The expression proportion of KANK2-L isoform was positively correlated with USP39 mRNA expression in tumor tissues (Pearson Correlation test). C Kaplan–Meier OS curves of in-house HCC patients based on USP39 expression (high vs. low, defined as tumor/non-tumor > 1) and KANK2-L percentage (high vs. low, defined as tumor(%)/non-tumor(%) > 1). D WB assay revealed KANK2 protein reduction in USP39 knockdown cells. E WB analysis of adjacent non-tumor (NT) and tumor (T) tissue lysates from HCC patients with USP39 and KANK2 antibodies. β-Actin was used as a loading control. F Polyribosome profile analysis revealed that KANK2-L isoform enhanced the translation of KANK2 protein. G Tet-KANK2 was introduced to USP39-deficient PLC-8024 cells (up). Two Tet-On shRNAs targeting KANK2-L (tetshKL) and KANK2-S (tetshKS) were introduced into USP39-overexpressing PLC-8024 cells (down). Foci formation assay was performed to assess the growth of the indicated cells. Representative images and statistical results are shown (n = 3). Mean ± SD. P values by paired (A) or unpaired (G) Student’s t-test. *P < 0.05, **P < 0.01, ns: not significant.

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