Regulation of Bmi-1 expression by AMPK and its effect on the proliferation of osteosarcoma cells

Adenosine monophosphate-activated protein kinase (AMPK) is modulated by AMP/ATP ratio and is the "detector" for cellular energy. Its activation in various tumor cells can inhibit cell proliferation and migration. Study has found the over-expression of B cell specific murine leukemia viral integration site-1 (Bmi-1). This study thus investigated the regulation of AMPK on Bmi-1 in human osteosarcoma cell line 143B, and the role of AMPK and Bmi-1 on tumor migration and metastasis. 143B cells were cultured and activated for AMPK by different concentrations of AICAR (0.1 mmol/L, 0.5 mmol/L and 1.0 mmol/L). MTT assay was used to detect the proliferation activity of cells after AICAR intervention. Western blotting was employed to test protein levels of AMPK and Bmi in 143B cells. Cellular mRNA expression of Bmi was quantified by RT-PCR. Different dosages of AICAR significantly inhibited cell proliferation at all time points. 0.5 mmol/L ACAIR had the most significant inhibitory effect (P<0.05). AMPK was activated in 143B cells 1 hour after intervention, with reaching a peak level at 6 hours, followed by gradual decrease until 24 hours. The expression of Bmi was also decreased after AICAR treatment, with the most significant effect in 0.5 mmol/L group (P<0.05). AMPK can inhibit proliferation and metastasis of osteosarcoma cells via suppressing Bmi-1 expression.