KIF26B promotes cell proliferation and migration through the FGF2/ERK signaling pathway in breast cancer

Background: Many studies have suggested that high KIF26B expression is directly linked to poor prognostic outcomes in breast cancer. However, the exact role of KIF26B in breast cancer progression is not fully understood. In this study, we aimed to explore the function and mechanism of KIF26B in breast cancer progression. Methods: Quantitative real-time PCR and immunohistochemistry analysis were used to detect KIF26B expression in breast cancer cell lines and patient samples. Cell proliferation was assessed by CCK-8 assay, and cell migration and invasion were evaluated by wound healing assay and transwell assay. Western blot analysis was carried out to assess the underlying molecular mechanisms. Tumor formation and metastasis were determined by in vivo mouse experiments. Results: KIF26B levels were significantly increased in breast cancer cells and patient samples. KIF26B level correlated with tumor size, TNM grade, and differentiation in patients with breast cancer. Overexpressing KIF26B in vitro promoted breast cancer cell proliferation and migration by activating FGF2/ERK signaling, while silencing KIF26B had the opposite effects. Similarly, KIF26B knockdown repressed tumor formation and metastasis in nude mice. Conclusion: KIF26B promoted the development and progression of breast cancer and might act as a potential therapeutic target for treating breast cancer.