EFFECTS OF SULFORAPHANE ON APOPTOSIS AND PI3K/AKT/MTOR PHOSPHORYLATION PATHWAY IN COLORECTAL CANCER CELLS

Objective: To investigate the effects of sulforaphane (SFN) on the phosphorylation signal pathway of phosphatidylinositol-3kinase (PI3K)/white kinase B (Akt)/mammalian rapamycin target protein (mTOR) in colorectal cancer cells induced by SFN. Methods: An SW620 colorectal cancer cell line was selected and cultured until the cell grew to about 90% of the bottom of the culture bottle. The cells in the logarithmic growth phase were inoculated into a 96-well plate and treated with low, medium, and high doses of SFN (10, 30, and 60 mg/L, respectively) after adherence. The proliferation inhibition rate of SW620 cells was detected by a CCK8 test, and the apoptosis of SW620 cells was observed by IP staining. The expressions of the proapoptotic protein Bax, the antiapoptotic protein Bcl-2, PI3K, p-Akt, and p-mTOR were detected by blot, and the effects of SFN on apoptosis and the PI3K/Akt/ mTOR phosphorylation pathway were analyzed. Results: The inhibition rate of cell proliferation in each group increased with the extension of time, and the proliferation inhibition rate in the experimental group was significantly higher than that in the control group. The cell proliferation inhibition rate of the experimental group increased with the increase of the dose at each time point, and the difference was statistically significant (P<.05). The apoptosis rate of the experimental group was significantly higher than that of the control group. The apoptosis rate of the experimental group increased as the dose increased, and the difference was statistically significant (P<.05). The number of G0/G1 phase cells in the experimental group was significantly higher than that in the control group (P<.05). It is suggested that SFN can make SW620 cells stay in the G0/G1 phase and induce apoptosis. The level of the proapoptotic protein Bax in the experimental group was significantly higher than that in the control group and increased as the dose increased. The level of the antiapoptotic protein Bcl-2 in the experimental group was significantly lower than that in the control group, and the difference was statistically significant (P<.05). The levels of PI3K, p-Akt, and p-mTOR in the experimental group were considerably lower than those in the control group, and the difference was statistically significant (P<.05). Conclusion: SFN can accelerate the damage of colorectal cancer cells and induce apoptosis, which may be related to the inhibition of the PI3K/Akt/mTOR phosphorylation pathway.