EMODIN INHIBITS THE PROLIFERATION AND PROMOTES THE APOPTOSIS OF GASTRIC CANCER CELLS BY REGULATING PRL-3 EXPRESSION AND ACTIVATING THE PI3KAKT SIGNALING PATHWAY

Fang Li¹, Yang Qin¹, Juan Zhu¹, Hongning Pan^2*

¹Department of Nursing, Jiangsu Vocational College of Medicine, Yangcheng City, 224005, Jiangsu Province, China - ²Teaching Supervision Room, Jiangsu Vocational College of Medicine, Yangcheng City, 224005, Jiangsu Province, China

Objective: To analyze how emodin impacts the proliferation and apoptosis of gastric cancer cells by regulating the expression of PRL-3 and activating the PI3Kakt signaling pathway.

Methods: During their logarithmic growth phase, SGC-7901 cells were cultured in a 96-well culture plate and divided into a control group and an experimental group. The experimental group was divided into 4 groups: a 10 μm emodin group, a 20 μm emodin group, a 30 μm emodin group, and a 40 μm emodin group. After the cells adhered to the wall, the emodin medium was changed. The control group was added with the same amount of culture medium, and the experimental group was added with different concentrations of emodin. The a570nm OD value was detected using an enzyme-labeled instrument at 24h, 48h, and 72h, and the proliferation inhibition rate of each group was calculated. The apoptotic cells, necrotic cells, and living cells were recorded under a fluorescence microscope, and the apoptosis rate of tumor cells was calculated. After 24 hours of emodin treatment, RNA and total protein were extracted, and PRL-3 mRNA, PRL-3 protein, and PI3Kakt signaling pathway related eggs were detected according to the expression of white and its downstream molecules. Emodin inhibits the proliferation and promotes the apoptosis of gastric cancer cells by regulating the expression of PRL-3 and activating the PI3Kakt signaling pathway.

Results: The proliferation inhibition rate of SGC-7901 cells in the emodin groups was significantly higher than the control group rate; furthermore, it increased over time. At the same time point, the proliferation inhibition rate of human gastric adenocarcinoma SGC-7901 cells increased with increases in dosage, and the difference was statistically significant (P<0.05). The apoptosis rate of SGC-7901 cells in the emodin groups was also significantly higher than the control group rate, and the apoptosis rate of SGC-7901 cells in the emodin groups also increased with increases in dosage (P<0.05). The expression of PRL-3 mRNA in the emodin groups was significantly lower than expression in the control group, and the expression of PRL-3 mRNA decreased with increases in dosage (P < 0.05). The PRL-3 protein level in the emodin groups was significantly lower than the level in the control group, and the PRL-3 protein level decreased with increases in dosage; the difference was statistically significant (P<0.05). The levels of p-Akt (thr-308) and p-Akt (ser473) in the emodin groups were significantly lower than the control group levels, and the levels of p-Akt (thr-308) and p-Akt (ser473) decreased with increases in dosage; the difference was statistically significant (P<0.05). The Bcl-2 protein level in the emodin groups was significantly lower than the control group level, and the Bax protein level was significantly higher than the control group level; Bcl-2 levels decreased with increases in dosage, and Bax levels increased with increases in dosage. Again, the differences were statistically significant (P<0.05).

Conclusion: Emodin can inhibit the proliferation and induce the apoptosis of gastric cancer cells in a time- and concentration-dependent manner. During this process, PRL-3 mRNA and protein levels decrease. Emodin regulates the proteins related to the PI3Kakt signaling pathway and participates in the mechanism promoting the apoptosis of gastric cancer cells.