Abstract
The treatment of hepatocellular carcinoma (HCC) is still relatively lacking, the prognosis is poor, and the potential mechanism of carcinogenesis has not been thoroughly studied. In this study, Ubiquitin-conjugating enzyme E2K (UBE2K) transcript levels in HCC patients were up-regulated in two databases, GEO and TCGA. External validation was performed using Western blot experiments. Compared to normal liver cells, UBE2K was upregulated in HCC cell lines. The survival curve and prognosis model revealed that the expression of UBE2K was of high prognostic value in patients with HCC. Transwell assay, wound healing assay and sphere formation assay were used to evaluate the effects of knockdown and overexpression of UBE2K on HCC cells. Overexpression of UBE2K promoted the invasion, migration and stemness of HCC cells, while knocking down UBE2K attenuated the invasion, migration and stemness of HCC cells. Then, through a series of functional analysis (GO and KEEG), it was found that UBE2K played an important role in mRNA processing. We speculate that UBE2K may be involved in HCC progression through its own N6-methyladenosine modification. We therefore used a global methylation inhibitor (3-deazaadenosine) to treat HCC cells and found a gradient increase in the mRNA level of UBE2K. Collectively, the results suggest that UBE2K may be a promising molecular target for the treatment of HCC.
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