AAVC-I promotes apoptosis of human oral squamous cell carcinoma through the mitochondrial pathway.

This study aimed to explore the role and possible mechanism of component I from agkistrodon acutus venom (AAVC-I) in promoting the apoptosis of oral squamous cell carcinoma (OSCC). HN4 cells (a human OSCC cell line) were randomly divided into four experimental groups: low AAVC-I (2.5 μg/mL) group, medium AAVC-I (5 μg/mL) group and high AAVC-I (10 μg/mL) group, as well as control group (AAVC-I, 0 μg/mL). AVVC-I was dissolved in RPMI-1640 medium and added to the culture wells at different concentrations when tumor cells had reached the logarithmic growth phase. After 24 hours, cells were harvested and the inhibitory rate of cell proliferation and the mitochondrial membrane depolarization were measured. Western blotting was used to detect the expression levels of cytochrome c, Bcl-2 associated X protein (Bax), and caspase-3 in the cellular cytoplasm either containing mitochondria or following the removal of mitochondria. Cellular apoptosis was detected by flow cytometry. Compared to the control group, AAVC-I treatment not only inhibited NH4 growth, but also upgraded the expression of caspase-3 in NH4 cells. Meanwhile, it was observed that Bax translocation to mitochondria and cytochrome c release into the cytosol increased in AAVC-I treatment. This indicated that AAVC-I could disrupt mitochondrial membrane depolarization and result in cellular apoptosis, and the apoptosis rate of NH4 increased with the concentration of AAVC-I. The data suggested that AAVC-I promotes the apoptosis of HN4 cells through the mitochondrial pathway in a dose-dependent manner, which provides experimental data and new ideas for future research and clinical treatment options for OSCC.