Ascorbyl stearate stimulates cell death by oxidative stress-mediated apoptosis and autophagy in HeLa cervical cancer cell line in vitro

In this study, Asc-s was evaluated for anti-cancer effect using cervical cancer cells (HeLa). Results determine that Asc-s treatment-induced dose-dependent inhibition of proliferation of HeLa cells and induced apoptosis. Flow-cytometry analysis shows Asc-s treatment-induced accumulation of cells at sub-G0/G1 stage of cell cycle and induced apoptosis as confirmed by DAPI, propodium iodide, and acridine staining in HeLa cells. Asc-s entered the cells and metabolized to ascorbate and stearate moieties, increased membrane permeability, and decreased membrane fluidity in HeLa cells. Asc-s treatment-induced dose-dependent increase in autophagy protein LC3-II, mRNA levels and decreased Nrf-2 levels in HeLa cells. It is hypothesized that both ascorbyl radical and stearoyl moieties of Asc-s induced cytotoxicity by generating reactive oxygen species (ROS) and modulating membrane fluidity/permeability leading to apoptosis/autophagy of HeLa cells. Thus, our findings demonstrate that Asc-s as anti-proliferative and apoptosis inducing compound in cervical cancer cells.