PURPOSE: To investigate the effect of omentin-1 on the proliferation and apoptosis of colon cancer stem cells and the underlying mechanism. METHODS: Colon cancer stem cells were obtained by indirect immune-magnetic beads cultured in serum-free medium, and identified by spheres formation assay, differentiation assay and flow cytometry. Colon cancer stem cells were divided into the control group, the omentin-1 group (1 μg/ml omentin-1), the omentin-2 group (2 μg/ml omentin-1), the omentin-LY group (1 μg/ml omentin-1 and 50 μM LY294002) and the LY group (50 μM LY294002). CCK-8 and flow cytometry were used to detect the proliferation and apoptosis, respectively. The cell proliferation was evaluated at 0, 1, 6, 24 and 48 hrs after the intervention by omentin-1. Western blot was performed to measure the effect of different concentrations of omentin-1 on phosphorylated Akt. RESULTS: The colon cancer stem cells were successfully sorted, and the content of CD133+ in colon cancer stem cells reached 80.3%. Omentin-1 inhibited the proliferation and promoted apoptosis of colon cancer stem cells in a dose and time-dependent manner, which could be strengthened by the PI3K/Akt inhibitor. CONCLUSION: Omentin-1 could inhibit the proliferation and promote apoptosis of colon cancer stem cells in vitro via the PI3K/Akt pathway.
PURPOSE: To investigate the effect of omentin-1 on the proliferation and apoptosis of colon cancer stem cells and the underlying mechanism. METHODS:Colon cancer stem cells were obtained by indirect immune-magnetic beads cultured in serum-free medium, and identified by spheres formation assay, differentiation assay and flow cytometry. Colon cancer stem cells were divided into the control group, the omentin-1 group (1 μg/ml omentin-1), the omentin-2 group (2 μg/ml omentin-1), the omentin-LY group (1 μg/ml omentin-1 and 50 μM LY294002) and the LY group (50 μM LY294002). CCK-8 and flow cytometry were used to detect the proliferation and apoptosis, respectively. The cell proliferation was evaluated at 0, 1, 6, 24 and 48 hrs after the intervention by omentin-1. Western blot was performed to measure the effect of different concentrations of omentin-1 on phosphorylated Akt. RESULTS: The colon cancer stem cells were successfully sorted, and the content of CD133+ in colon cancer stem cells reached 80.3%. Omentin-1 inhibited the proliferation and promoted apoptosis of colon cancer stem cells in a dose and time-dependent manner, which could be strengthened by the PI3K/Akt inhibitor. CONCLUSION:Omentin-1 could inhibit the proliferation and promote apoptosis of colon cancer stem cells in vitro via the PI3K/Akt pathway.