Abstract
Colorectal cancer (CRC) is a formidable threat to human well-being, characterized by a largely enigmatic occurrence and progression mechanism. A growing body of literature has underscored the potential influence of propofol, a frequently administered anesthetic, on clinical outcomes in malignant tumor patients. However, the precise molecular mechanisms underlying the impact of propofol on the progression of CRC have yet to be fully elucidated. This study reveals a notable upregulation of LINC01133 expression in CRC cells subsequent to propofol treatment, which is mediated by FOXO1. Subsequently, a series of experiments were conducted to elucidate the role and mechanisms underlying propofol-induced LINC01133 in CRC development. Our study uncovers that the upregulation of LINC01133 exerts a substantial inhibitory effect on the proliferation, migration, and invasion of CRC cells. Further investigation revealed that LINC01133 can attenuate the proliferation, invasion, and migration of CRC cell lines through the miR-186-5p/NR3C2 axis. Results from in vivo experiments unequivocally demonstrated a significant reduction in the growth rate of subcutaneous implant tumors upon LINC01133 overexpression in CRC cells. These findings posit that propofol induces LINC01133 expression, leading to the inhibition of CRC progression. This revelation offers a novel perspective on propofol's antitumor properties and underscores the potential of LINC01133 as a promising therapeutic target for CRC.