Ciprofol suppresses glycolysis and EMT in colorectal cancer cells by activating APC to modulate the Wnt/β-catenin signaling pathway.
Ciprofol, an innovative anesthetic derived from propofol, has not yet been studied in detail regarding its effects in colorectal cancer (CRC). This study mainly explored the effects of Ciprofol on the epithelial-mesenchymal transition (EMT) process, glycolysis, and the Wnt/β-catenin signaling pathway in CRC cells. Through in vitro and in vivo experiments, we successfully demonstrated that Ciprofol can inhibit the proliferative capacity of CRC cells and tissues. It can also suppress the invasion, metastasis, and EMT process of CRC cells. In addition, treatment with Ciprofol decreased the oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) in CRC cells, thereby inhibiting cellular glycolysis. However, knockdown of APC could reverse the effects of Ciprofol. Regarding the mechanism, overexpression of APC was able to activate the Wnt/β-catenin signaling pathway. Ciprofol could activate the expression of APC, subsequently activating the Wnt/β-catenin signaling pathway. The addition of Derivative83 could reverse Ciprofol - mediated regulation of this pathway. This study still has certain limitations. For example, the verification through clinical trials, as well as issues such as the safety and efficacy of ciprofol, remain the key focuses of future research.