Background and Aims The circular RNA KIF4A (circKIF4A) has been found to play an important role in the malignant progression of various tumors. However, the biological role of circKIF4A in colorectal cancer has not been reported yet. Therefore, this study was conducted to investigate the effects and mechanisms of circKIF4A on the biological behavior of colorectal cancer.Methods The expressions of circKIF4A in different colorectal cancer cell lines and colonic mucosal epithelial cells as well as in colorectal cancer tissues and adjacent normal tissues were detected using qRT-PCR. After knocking down the expression of circKIF4A in colorectal cancer SW620 cells using siRNA, the cell growth, colony formation, invasion ability, as well as changes in the intracellular ratio of total glutathione (T-GSH) to oxidized glutathione (GSSG) and the expression of ferroptosis inhibitor protein SLC7A11 were detected. The target microRNAs (miRNAs) of circKIF4A and downstream target genes were predicted and analyzed using bioinformatics software and dual-luciferase reporter gene assay, and validation experiments were also perfromed.Results Compared to normal colonic epithelial cells and adjacent tissue, the expressions of circKIF4A were significantly upregulated in different colorectal cancer cell lines and cancer tissue (all P<0.05). Knockdown of circKIF4A resulted in significantly decreased cell growth, colony formation, invasion ability, intracellular T-GSH/GSSG ratio, and SLC7A11 protein expression in SW620 cells (all P<0.05). Prediction and analysis revealed the presence of a miR-515-5p binding site on the circKIF4A sequence, and SLC7A11 was identified as a downstream target gene of miR-515-5p. Validation results showed that miR-515-5p overexpression with simultaneous circKIF4A suppression had the most the inhibitory effect on SLC7A11 protein expression in SW620 cells among different treatments (P<0.05).Conclusion The expression of circKIF4A is upregulated in colorectal cancer cells and promotes the growth and invasion of colorectal cancer cells. Its mechanism may be associated with ferroptosis mediated by the circKIF4A-miR-515-5p-SLC7A11 axis.