Aberrant KIF23 expression is associated with adverse clinical outcome and promotes cellular malignant behavior through the Wnt/β-catenin signaling pathway in Colorectal Cancer

Purpose: The aim of the present study was to reveal the clinicopathological significance and prognostic role of kinesin family member 23 (KIF23) in colorectal cancer (CRC) and characterize its biological function and the underlying mechanisms. Methods: Bioinformatics analysis, immunohistochemistry, Western blot and qRT-PCR were utilized to investigate the expression of KIF23 in CRC tissues. The CCK-8 assay, wound healing assay and Matrigel assay were used to detect cell proliferation, migration and invasion in vitro. Western blot, immunofluorescence staining and cell function experiment were performed to explore the underlying mechanism. Results: The overexpression of KIF23 was associated with T stage, N stage, M stage and TNM stage, and CRC patients with high KIF23 expression had a worse prognosis. KIF23 knockdown inhibits CRC cells proliferation, migration and invasion in vitro. The mechanism study determined that KIF23 activates the Wnt/beta-catenin signaling pathway by promoting the nuclear translocation of beta-catenin to regulate the malignant behavior of CRC cells. Conclusion: These results suggest that KIF23 may act as a putative oncogene and a potential therapeutic target in CRC.

Automated summary

The study revealed that high expression of KIF23 is associated with the malignancy and prognosis of CRC, and its knockdown can inhibit cell proliferation, migration, and invasion. Mechanistic studies showed that KIF23 regulates the malignant behavior of CRC cells by activating the Wnt/beta-catenin signaling pathway.