A Mechanism For The Growth Inhibition Of Cervical Cancer Cell Line Hela Cells By Amygdalin

Objective: Human cervical cancer is the second malignancy occurs in womenworldwide. Apoptosis is an evolutionarily highly conserved form of cell death, andfind effective apoptosis-inducing method is one important strategy to treat cancer.Amygdalin is a natural medicine, which has anti-tumor activity, but the therapeuticeffects of amygdalin on cervical cancer in vivo and in vitro have not been reported. Inthis study, we studied in vitro and in vivo experiments, as well as gene chiphigh-throughput screening technology to explore antitumor effects and mechanism ofamygdalin in HeLa cells, and improve the mechanism of the anti-tumor effect.Methods: MTT assay was used to detect different concentrations of amygdalinon the survival rate of HeLa cells and FL cells; DAPI staining was applied to observeapoptosis; flow cytometry was used to show apoptosis rate of HeLa cells treated bydifferent concentrations of amygdalin; apoptosis-related protein expression wasdetected by Western Blot. Tumor xenografts transplanted by human uterine cervixcancer HeLa cells were used to evaluate the antitumor effect of amygdalin. Humangenome-wide chips U133were applied to screen the differentially expressed genescaused by amygdalin in HeLa cells.Results: In vitro experiments confirmed that amygdalin was capable of inducinghuman cervical carcinoma HeLa cell apoptosis in a dose-dependent manner;accompanied by increased ratio of Bax and Bcl-2, as well as the activation ofcaspase-3enzyme. Amygdalin induced apoptosis process through targeted regulationof Bax and Bcl-2expression, causing mitochondrial membrane damage, eventuallyleading to the cleavage of caspase-3activation, starting mitochondrial apoptosispathway. The human genome U133chip test results showed that expressions of573genes changed between amygdalin-treated group and negative control group, the JNK/c-Jun pathway played a role in apoptosis of HeLa cells induced by amygdalin.Conclusion: In vitro study showed amygdalin could inhibit HeLa cell viability ina dose dependent manner, amygdalin induced HeLa cell apoptosis by intrinsicmitochondrial pathway. In vivo study showed that amygdalin could inhibit the growthof HeLa cell xenografts by inducing apoptosis. Chip study showed that expressions of573genes changed and JNK/c-Jun pathway involved in amygdalin-induced apoptosis.