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. 2023 Sep 22;8(18):e162893. doi: 10.1172/jci.insight.162893

Figure 2. 3′UTR shortening enhances the oncogenic potential of MORC2 in KIRC by upregulating MORC2.

Figure 2

(A) The schematic diagram indicating the proximal polyA sites of MORC2 and UCK2. (B) Immunoblotting was performed to evaluate the expression of Flag-UCK2, Flag-MORC2, and GFP in Caki-1 and A498 cells transfected with indicated plasmids. (C) CCK8 assays were performed to evaluate the proliferation rate of Caki-1 cells and A498 cells transfected with short or long 3′UTR UCK2 plasmid (n = 3). (D) CCK8 assays were performed to evaluate the proliferation rate of Caki-1 cells and A498 cells transfected with short or long 3′UTR MORC2 plasmid (n = 3). (E) Colony formation assays were performed and quantitatively analyzed to evaluate the clonogenicity of Caki-1 cell and A498 cells transfected with short or long 3′UTR UCK2 plasmid (n = 3). (F) Colony formation assays were performed and quantitatively analyzed to evaluate the clonogenicity of Caki-1 cell and A498 cells transfected with short or long 3′UTR MORC2 plasmid (n = 3). (G) Soft agar assays were performed and quantitatively analyzed to evaluate the clonogenicity of Caki-1 cell and A498 cells transfected with short or long 3′UTR MORC2 plasmid (n = 3). (H and I) In vivo xenograft tumor formation experiment was performed (H) and quantitatively analyzed (I) with control, short 3′UTR, or long 3′UTR MORC2 stably expressed Caki-1 cells (n = 5 per group). All data represent the mean ± SD. Two-tailed t test or 1-way ANOVA with Tukey multiple-comparison test analyses were performed. *P < 0.05; **P < 0.01; ***P < 0.001.