Background: Hepatocellular carcinoma (HCC) is a complicated disease with a poor prognosis and high mortality rates. The prevention, control, diagnosis, and treatment of liver cancer have become vital focuses in healthcare research.
Aim: This study aimed to evaluate the in vitro effect of taurine (Tau) on the expression of miR-122-5p that targets some limiting glycolytic enzymes and affects the overall glycolytic pathway in HepG2 cells.
Method: IC and the inhibitory effect of Tau on cell proliferation were measured after 48 h by MTT assay. Then, the mRNA expressions of some apoptosis-related genes P53, BAX, Caspase-3, and Bcl-2 were measured using quantitative real-time (qRT-PCR) and the protein levels were confirmed by enzyme-linked immunosorbent assay (ELISA). The activities of some antioxidant's biomarkers were assessed. The gene expression of miR-122-5p that targets some limiting glycolytic enzymes; Aldolase and Lactate dehydrogenase (LDH), were evaluated after treatment with Tau for 48 h.
Results: A Significant inhibition in the proliferation of HepG2 was encountered after treatment with Tau in a dose-dependent manner. Moreover, the expression of apoptotic genes p53, Bax, and Caspase-3 exhibited a significant upregulation, while Bcl-2 showed a significant downregulation. These alterations in the expression levels were also confirmed on the protein level. The antioxidant activities of GPx, CAT, and NO were significantly elevated versus untreated control. Also, a significant increase in the expression level of miR-122-5p was observed after treatment with Tau affecting the metabolic activity of HCC cells. Concomitantly, a significant inhibition in ALDOA protein and the hallmark of glycolytic enzymes LDH and Aldolase were observed.
Conclusions: These observations showed that taurine inhibits HepG2 cell proliferation and restores the expression of miR-122-5p which inhibits the hallmark glycolytic enzymes and ultimately the metabolic activity of HCC cells. Tau is assumed to be a promising and effective antitumor therapy of HCC.
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