Abstract
β-enolase (ENO3) is a metalloenzyme that functions during glycolysis and has been revealed ectopic expression in different cancers. However, the function and underlying modulatory mechanisms of ENO3 in hepatocellular carcinoma (HCC) are still elusive. Here, we discovered that ENO3 was remarkably down-regulated in human HCC tissue in contrast to those in noncancerous tissue. Moreover, low expression of ENO3 was related to the poor prognosis of HCC patients. Overexpression of ENO3 suppressed proliferative, migratory, and invasive abilities of HCC cells both in vitro and in vivo, whereas knocking down ENO3 led to the opposite effect. In addition, we revealed that ENO3 repressed the epithelial-mesenchymal transition (EMT) process with its biomarker variations. Mechanistic research unveiled that ENO3 suppressed the Wnt/β-catenin signal, which subsequently modulated the transcription of its target genes associated with the proliferation and metastasis capacity of HCC cells. Taken together, our study uncovered that ENO3 acted as a tumor inhibitor in HCC development and implied ENO3 as a promising candidate for HCC treatment.
Highlights
hepatocellular carcinoma (HCC), the major form of primary hepatic carcinoma, is one of the most common cancer types and ranks fourth in terms of tumor-related mortality worldwide (Llovet et al, 2021)
The K-M survival assay of TCGA and ICGC databases displayed that HCC sufferers with higher expression of ENO3GFP-Puro plasmid (ENO3) exhibited more prolonged OS compared with sufferers with low expression of ENO3 (Figure 1B)
These data strongly suggested that ENO3 was downregulated in HCC, and the low expression was related to undesirable clinical outcomes in the HCC patients, which provided prima facie evidence that ENO3 might be pivotal for HCC
Summary
HCC, the major form of primary hepatic carcinoma, is one of the most common cancer types and ranks fourth in terms of tumor-related mortality worldwide (Llovet et al, 2021). Different risk factors, such as HBV or HCV infections, cirrhosis, autoimmune hepatitis, nonalcoholic fatty liver disease, and alcohol abuse, may facilitate HCC progression (Villanueva, 2019; Rebouissou and Nault, 2020; Llovet et al, 2021). It’s imperative to define the modulatory causal links of HCC and determine new therapeutic targets
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