Abstract
Upregulated ubiquitin-conjugating enzyme E2M (UBE2M) is associated with poor prognosis in malignancies; However, the phenotype and mechanism of action of UBE2M in hepatocellular carcinoma (HCC) remain elusive. Here, we report that UBE2M is overexpressed and correlated with poor prognosis in HCC patients. The UBE2M level is an independent prognostic factor for HCC patients. UBE2M knockdown inhibits HCC cell proliferation, migration, and invasion, whereas its overexpression has an opposite effect. Mechanistically, upregulated UBE2M exerts oncogenic effects by translocation of accumulated β-catenin from the cytoplasm to the nucleus, thus activating downstream β-catenin/cyclin D1 signaling. In summary, our study demonstrates a notable role of UBE2M in promoting the growth of HCC, providing a novel strategy for HCC prevention and treatment.
Highlights
Hepatocellular carcinoma (HCC) represents one of the most common malignancies and the third leading cause of cancer-related deaths worldwide [1]
We found that the ubiquitin-conjugating enzyme E2M (UBE2M) expression in hepatocellular carcinoma (HCC) tissues was significantly higher than that in matched tumor-free tissues using a pairwise comparison analysis (7.28 ± 3.66 vs. 4.02 ± 3.56; Figure 1B, 1C and Supplementary Figure 1; P < 0.001), which is consistent with the data in The Cancer Genome Atlas (TCGA; Figure 1D, P < 0.0001)
Further analysis revealed that sixty-two patients have upregulated UBE2M expression in HCC compared to the non-tumor tissues
Summary
Hepatocellular carcinoma (HCC) represents one of the most common malignancies and the third leading cause of cancer-related deaths worldwide [1]. In canonical Wnt/β-catenin signaling, aberrant β-catenin expression leads to a variety of diseases, including cancers [4, 5]. Under stimulated conditions, accumulated β-catenin translocates from the cytoplasm into the nucleus where it acts as a co-activator of the Tcell factor/lymphoid enhancer factor family transcription factors, resulting in transcription of multiple downstream genes involved in cell cycle www.aging-us.com progression, like cyclin D1 and c-Myc [8, 9]. Since emerging evidence suggests that ubiquitin-conjugating enzymes (E2) play a critical role in both tumorigenesis and tumor progression via regulating β-catenin expression [10,11,12,13], it has raised the question whether other members of the E2 family affected tumorigenesis
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