Adiponectin regulates the malignant biological behavior of endometrial cancer cells via AMPK/mTOR signal pathway

Purpose: To study the mechanism by which adiponectin regulates the malignant biological behavior of endometrial cancer cells. Methods: RL95-2 cells were cultured and re-suspended in complete medium. A preliminary study showed that adiponectin (20 μg/mL) has the most inhibitory effect on cellular proliferation. The cells were divided into control group, 20 μg/mL adiponectin group, and 20 μg/mL adiponectin + 10 μmol/L AMPK inhibitor group, with 4 repeat wells set up for each group. Cell proliferation, apoptosis, invasion and migration ability, as well as the expression levels of MMP-9, Bcl-2, p-AMPK, p-mTOR and p-4ebp1 were determined using standard procedures. Results: Cell proliferation was significantly higher in the 20 μg/mL adiponectin group than in the 10 μg/mL adiponectin group (p < 0.05). Relative to the control group, apoptosis and p-AMPK expression level in the 10 μg/mL adiponectin group increased, while cell invasion and migratory potential, as well as expression levels of MMP-9, Bcl-2, p-mTOR and p-4ebp1 declined significantly (p < 0.05). The apoptosis and expression level of p-AMPK in the 20 μg/mL adiponectin + 10 μmol/L AMPK inhibitor group decreased, while cell invasion, migratory ability, and amounts of MMP-9, Bcl-2, p-mTOR and p- 4ebp1 were elevated, relative to the 20 μg/mL adiponectin group (p < 0.05). Conclusion: Adiponectin promotes apoptosis of endometrial cancer cells via AMPK/mTOR signaling pathway, and inhibits cell proliferation, invasion and migration. Thus, adiponectin has the potential to exert anti-tumor effect in humans.