ArticleBMC gastroenterology2025
KIF3C inhibits the progression and proliferation of colorectal cancer.
Article in BMC gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
backgroundEvidence indicated that KIF3C, a member of the kinesin superfamily of motor proteins, exhibits significant upregulation across various cancer types. Consequently, its impact on cancer advancement, including cell proliferation, migration, and invasion, is evident. Nonetheless, the comprehension of KIF3C's expression and role in colorectal cancer (CRC) remains limited.
methodsImmunohistochemistry was used to evaluate the presence of KIF3C in CRC. The expression levels of KIF3C were assessed in CRC cells through western blot analysis (WB) and real-time polymerase chain reaction (RT-qPCR). KIF3C was knockdown and overexpressed using lentiviral vectors in the human CRC cell lines SW-480, HCT-116, and SW-620. In vitro experiments such as transwell assays, scratch wound healing, colony formation assays, counting cell CCK-8, and signaling pathway experiments were conducted to validate the KIF3C function in CRC cells.
resultsWe demonstrated that KIF3C is highly expressed in cells and tissues of CRC, and this expression is closely associated with tumor prognosis. It was shown that KIF3C knockdown significantly inhibited tumor cell proliferation and migration in CRC cells. Additionally, the KIF3C signaling pathway experiment in this study promoted the CRC progression by upregulating the PI3K/AKT, Bax, and Bcl-2 pathways.
conclusionsKIF3C knockdown promoted CRC proliferation, as it could be a potential therapeutic target for treating CRC.
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