Min-wen Ha1, Yuan Yuan. 1. Cancer Institute, First Affiliated Hospital of China Medical University, Shenyang 110001, China.
Abstract
OBJECTIVE: To study the effect of allicin on cell cycle of human gastric cancer cell lines, MGC-803 and SGC-7901, and its possible mechanisms. METHODS: The gastric cancer cell lines MGC-803 and SGC-7901 were treated with allicin. Proliferation inhibitory rate was detected by trypan-blue exclusion. Morphologic changes were observed by electron microscopy. The cell cycle was examined by flow cytometry and Giemsa staining. Expression of p21WAF1, p16INK4 protein and mRNA was detected by immunohistochemistry and RT-PCR. RESULTS: The gastric cancer cells were inhibited after exposure to allicin for 24 hr, The IC50 was 6.4 microg/ml in MGC-803 cells and 7.3 microg/ml in SGC-7901cells. After exposure to allicin of 12 microg/ml for 24 hr, it caused the cytotoxic effect on the cells, including cellular membrane breakagy. After exposure to allicin of 3 microg/ml, 6 microg/ml and 9 microg/ml for 24 hr, compared with the control group, the proportion of cells in the G0/G1 phase was decreased and that in the G2/M phase was increased significantly (P < 0.01). After exposure to allicin of 6 microg/ml for 24 hr, compared with the control group, cell division index was much higher, suggesting that allicin could induce cell arrest in M phase. The expression levels of p21WAF1 and p16INK4 protein and mRNA in MGC-803 cells and p21WAF1 protein and mRNA in SGC-7901 cells were markedly up-regulated. CONCLUSION: Allicin induce cell arrest of gastric cancer in M phase, which may be related to the up-regulated expression of p21WAF1 and p16INK4 genes.
OBJECTIVE: To study the effect of allicin on cell cycle of humangastric cancer cell lines, MGC-803 and SGC-7901, and its possible mechanisms. METHODS: The gastric cancer cell lines MGC-803 and SGC-7901 were treated with allicin. Proliferation inhibitory rate was detected by trypan-blue exclusion. Morphologic changes were observed by electron microscopy. The cell cycle was examined by flow cytometry and Giemsa staining. Expression of p21WAF1, p16INK4 protein and mRNA was detected by immunohistochemistry and RT-PCR. RESULTS: The gastric cancer cells were inhibited after exposure to allicin for 24 hr, The IC50 was 6.4 microg/ml in MGC-803 cells and 7.3 microg/ml in SGC-7901cells. After exposure to allicin of 12 microg/ml for 24 hr, it caused the cytotoxic effect on the cells, including cellular membrane breakagy. After exposure to allicin of 3 microg/ml, 6 microg/ml and 9 microg/ml for 24 hr, compared with the control group, the proportion of cells in the G0/G1 phase was decreased and that in the G2/M phase was increased significantly (P < 0.01). After exposure to allicin of 6 microg/ml for 24 hr, compared with the control group, cell division index was much higher, suggesting that allicin could induce cell arrest in M phase. The expression levels of p21WAF1 and p16INK4 protein and mRNA in MGC-803 cells and p21WAF1 protein and mRNA in SGC-7901 cells were markedly up-regulated. CONCLUSION:Allicin induce cell arrest of gastric cancer in M phase, which may be related to the up-regulated expression of p21WAF1 and p16INK4 genes.
Authors: Wamidh H Talib; Dima Awajan; Reem Ali Hamed; Aya O Azzam; Asma Ismail Mahmod; Intisar Hadi Al-Yasari Journal: Molecules Date: 2022-08-25 Impact factor: 4.927