In vitro analysis on inhibitory effect of sodium arsenite combined with astragaloside IV on HepG2 liver cancer cells

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From the in vitro level, this paper explores the synergistic inhibitory effects and mechanisms of sodium arsenite (NaAsO2) and astragaloside IV(AS-IV) on HepG2 cells. By screening the optimal concentration of each drug, the authors tested the combined and separate effects of the two drugs on HepG2 cell proliferation, migration and invasion, cell cycle and apoptosis, as well as key genes and proteins of the PI3K/AKT/mTOR pathway (PI3K, p-PI3K, AKT, p-AKT, mTOR, and p-mTOR). The CCK-8 test and Transwell tests show that: the separate and joint uses of NaAsO2 and AS-IV reduced the viability and migration of cells to different degrees (p all < 0.05). The scratch test results show that: although the migration rate in each treatment group declined, only NaAsO2 + AS-IV group witnessed a significant decline in migration rate (p < 0.05); the percentage of S phase cells and apoptosis rate both increased significantly in each treatment group (p all < 0.05). GNGT1, PI3K, p-PI3K, AKT, p-AKT, mTOR, and p-mTOR were expressed in each treatment group; Among them, GNGT1 mRNA expression increased in each treatment group, while the expressions of PI3K, p-PI3K, AKT, p-AKT, mTOR and p-mTOR gene proteins decreased in each treatment group; the indices changed most significantly in the NaAsO2 + AS-IV group (p all < 0.05). By the inhibitory effect of each drug on HepG2 cells, the treatment groups could be ranked as NaAsO2 + AS-IV group > NaAsO2 group > AS-IV group; GNGT1 siRNA group had an opposite trend with each treatment group. From in vitro level, the above results confirm that NaAsO2 and AS-IV can inhibit HepG2, and the two drugs has a synergistic effect. In addition, the two drugs could inhibit HepG2 cells through the PI3K/AKT/mTOR signaling pathway; GNGT1 participates in the regulation of that signaling pathway.