In our study, MELK overexpression effectively attenuated xCT knockdown-induced suppression of tumor proliferation, migration, and stemness, and Akt/mTOR signaling activity was also significantly restored, indicating that xCT may control the tumorigenesis and progression of CRC via the MELK/Akt/mTOR signaling pathway. This evidence concerns the gene AKT1 and colorectal carcinoma.