期刊
JOURNAL OF CANCER
卷 12, 期 7, 页码 2030-2040出版社
IVYSPRING INT PUBL
DOI: 10.7150/jca.51565
关键词
KIF23; Colorectal cancer; Proliferation; Migration; Wnt/beta-catenin
类别
资金
- National Natural Science Foundation of China [NSFC-U1504818]
- Science and Technology Foundation of Henan Provincial [172102310152]
- Natural Science Foundation of Henan Province of China [182300410359]
- Medical Science and Technique Foundation of the Henan Province [201601029]
- Education Foundation of Henan Province [19A320020]
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.
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.
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