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Archive > Volume 33 Issue 7 > 2026,33(7):754-762. DOI:10.3872/j.issn.1007-385X.2026.07.006 Prev Next
Clinical Research
Mechanistic study of FOXK1 in promoting laryngeal squamous cell carcinoma progression by upregulating AKT2 expression
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Abstract:
Objective: To investigate the effects of FOXK1 on the proliferation, migration and invasion of laryngeal squamous cell carcinoma (LSCC) and the prognosis of patients, as well as its molecular mechanism. Methods: RT-qPCR and immunohistochemistry were applied to determine FOXK1 expression in LSCC tissues and TU177 cells, with subsequent analysis of its association with clinicopathological parameters and patient prognosis. FOXK1 overexpression and knockdown vectors were constructed and transfected into LSCC cell line TU177. MTS assay, colony formation assay, scratch wound healing assay, and Transwell assay were employed to detect changes in the malignant biological behaviors of cells. RT-qPCR was employed to detect the mRNA expression of epithelial- mesenchymal transition (EMT)-related factors, and Western blotting was used to detect the protein expression of PI3K/AKT signaling pathway-related proteins. Combined with bioinformatics prediction and functional rescue experiments, the regulatory effect of FOXK1 on AKT2 was verified. Results: FOXK1 was highly expressed in LSCC tissues and cells (P < 0.01), and was mainly localized in the cell nucleus; high FOXK1 expression was associated with a higher TNM stage (P < 0.05), and a lower 5-year survival rate (P < 0.05); FOXK1 overexpression significantly promoted the proliferation, migration and invasion of TU177 cells and induced EMT (P < 0.01 or P < 0.05), whereas FOXK1 knockdown produced the opposite effects; FOXK1 upregulated AKT2 expression and activated the PI3K/ AKT signaling pathway; knockdown of AKT2 partially reversed the promoting effects of FOXK1 overexpression on proliferation, migration, invasion and EMT progression (P < 0.01 or P < 0.05). Conclusion: FOXK1 is highly expressed in LSCC and is closely associated with tumor progression and poor prognosis. FOXK1 may activate the PI3K/AKT pathway by upregulating AKT2 expression, thereby inducing EMT and promoting the malignant biological behaviors of LSCC cells.
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