Exploring the Molecular Mechanism of Propofol-Mediated Inhibition of Colorectal Cancer through TM2D1-Mediated Ferroptosis
Objective:To investigate the molecular mechanism by which propofol inhibits colorectal cancer through TM2D1-mediated ferroptosis.Methods:The expression of TM2D1 in normal and colorectal cancer tissues was assessed.Human colorectal cancer SW480 cells were exposed to 50 μM propofol to examine cell viability.SW480 cells were transfected with an overexpressed TM2D1 vector and treated with propofol.The effects of propofol on cell viability,colony formation,cell proliferation,iron levels,ROS production,and ferroptosis were evaluated.Results:TM2D1 is highly expressed in colorectal cancer tissues.Propofol inhibited the viability of SW480 cells,leading to a significant down-regulation of TM2D1.Propofol also suppressed the proliferation and colony formation of colorectal cancer cells,while increasing cellular iron and ROS levels.Furthermore,propofol altered the expression of proteins associated with ferroptosis,including the up-regula-tion of CHAC1 and PTGS2,and the inhibition of GPX4 expression in CRC cells.Overexpression of TM2D1 blocked the effects of propofol on CRC cells,and the differences were statistically significant(P<0.05).Con-clusion:Propofol may induce ferroptosis in colorectal cancer cells by down-regulating TM2D1 expression.
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