Chinese Journal of Tissue Engineering Research ›› 2019, Vol. 23 ›› Issue (29): 4593-4598.doi: 10.3969/j.issn.2095-4344.1810

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Lutein regulates proliferation and apoptosis of gastric cancer stem cells through PI3K/AKT signaling pathway

Du Ruiling   

  1. Department of Traditional Chinese Medicine, Sichuan Provincial People’s Hospital, Chengdu 610072, Sichuan Province, China
  • Revised:2019-04-25 Online:2019-10-18 Published:2019-10-18
  • About author:Du Ruiling, MD, Associate chief physician, Department of Traditional Chinese Medicine, Sichuan Provincial People’s Hospital, Chengdu 610072, Sichuan Province, China

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Abstract:

BACKGROUND: Lutein can inhibit proliferation and promote apoptosis in cancer cells of various origins. However, there are no reports on the effect and mechanism of lutein on the proliferation and apoptosis of gastric cancer stem cells.
OBJECTIVE: To observe the effect of lutein on proliferation and apoptosis of gastric cancer stem cells and explore its possible mechanism.
METHODS: Gastric cancer stem cells were obtained from human gastric cancer cell line SGC-7901 in vitro. Flow cytometry was used to identify cell surface markers CD44 and CD24. Human gastric cancer stem cells were treated with 0, 20, 40, 80, and 160 mmol/L lutein for 24, 48, and 72 hours, respectively. Cell proliferation activity was detected by cell counting kit-8 method, to determine the optimal concentration and action time of lutein. Human gastric cancer stem cells were then divided into four groups: control group, 80 mmol/L lutein group, insulin-like growth factor 1 group, lutein+insulin-like growth factor 1 group, and given the corresponding treatments for 48 hours. Flow cytometry was used to detect cell apoptosis. The expressions of PI3K and Akt mRNA were detected by quantitative real-time PCR, and the expressions of PI3K, p-PI3K, Akt and p-Akt proteins were detected by western blot assay.
RESULTS AND CONCLUSION: (1) Gastric cancer stem cells derived from human gastric cancer SGC7901 cells cultured in vitro expressed CD44 and CD24. (2) Lutein at 80 and 160 mmol/L acting for 48 hours could achieve the best inhibitory effect (P < 0.05). As the half maximal inhibitory concentration (IC50) of lutein for 48 hours was 91.58 mmol/L, 80 mmol/L lutein acting for 48 hours was selected for subsequent experiments. (3) The proliferation activity of the cells was highest in the insulin-like growth factor 1 group and lowest in the lutein group, and there were significant differences between groups (P < 0.05). (4) The apoptotic rate was highest in the lutein group and lowest in the insulin-like growth factor 1 group, and there were significant differences between groups (P < 0.05). (5) The expressions of PI3K and Akt mRNA were highest in the lutein group and lowest in the insulin-like growth factor 1 group, and there were significant differences between groups (P < 0.05). (6) The expressions of p-PI3K and p-Akt protein in the lutein group were significantly lower than those in the control group and insulin-like growth factor 1 group, while the expressions of p-PI3K and p-Akt protein in the insulin-like growth factor 1 group were significantly higher than those in the other three groups (P < 0.05). These results suggest that lutein inhibits the proliferation and induces apoptosis of human gastric cancer stem cells by inhibiting the PI3K/Akt signaling pathway.

Key words: tumor stem cells, gastric cancer stem cells, lutein, signaling pathway, PI3K, Akt, cell proliferation, apoptosis

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