Objective: Liver cancer is one of the most common digestive system malignant solid tumors. Its incidence and mortality rates keep high, causing serious mental and economic burden. So far, the exact mechanism of liver cancer onset has not been fully elucidated. Metallothionein (MT) widely exists in various types of organisms with highly conserved structure. It contains the short peptide of cysteine and sulfur protein with high affinity to heavy metals, including cadmium, zinc, and copper. MT1M is an important member of MT family that has been verified to participate in regulating hepatocellular carcinoma, thyroid cancer, cervical cancer, and other tumors. However, MT1M expression and mechanism in hepatoma cells have not been fully elucidated.
Materials and methods: Hepatoma cell line HepG2 was divided into control and MT1M group. MT1M plasmid was constructed and transfected to MT1M group. Real-time PCR was used to test MT1M expression. MTT assay was applied to detect HepG2 proliferation. Flow cytometry was performed to determine HepG2 apoptosis. Caspase-3 activity was measured. Western blot was used to detect Bcl-2 and Bax protein levels.
Results: MT1M expression significantly increased after MT1M plasmid transfection compared with control (p < 0.05). MT1M group showed inhibited HepG2 proliferation, declined HepG2 apoptosis, enhanced Caspase-3 activity, reduced Bcl-2 protein level, and upregulated Bax protein compared with control (p < 0.05).
Conclusions: MT1M can suppress HepG2 proliferation and induce HepG2 apoptosis through downregulating Bcl-2, upregulating Bax, and enhancing Caspase-3 activity.