ERCC6L facilitates the progression of laryngeal squamous cell carcinoma by the binding of FOXM1 and KIF4A

The role of excision repair cross-complementation group 6-like (ERCC6L) has been reported in several cancers, but little is known about its expression and function in laryngeal squamous cell carcinoma (LSCC). In this study, the expression of ERCC6L in LSCC was determined by immunohistochemistry and its correlation with prognostic factors was analyzed. Furthermore, cytological functional validation elucidated the role and underlying mechanisms of ERCC6L dysregulation in LSCC. Our data revealed that ERCC6L expression was elevated in LSCC and it's correlated with TNM stage. In addition, ERCC6L knockdown LSCC cells showed decreased proliferation and migration, increased apoptosis, and reactive oxygen species (ROS). Mechanically, overexpression of ERCC6L promoted nuclear translocation of FOXM1 to facilitate direct binding to the KIF4A promoter and upregulated KIF4A expression. Furthermore, KIF4A knockdown attenuated the role of ERCC6L overexpression in promoting proliferation, migration, and tumorigenesis of LSCC cells. In summary, ERCC6L promoted the binding of FOXM1 and KIF4A in LSCC cells to drive their progression, which may be a promising target for precision therapy in this disease.

Automated summary

The expression and function of ERCC6L in laryngeal squamous cell carcinoma (LSCC) were investigated. ERCC6L was found to be upregulated in LSCC and correlated with TNM stage. Knockdown of ERCC6L resulted in decreased proliferation and migration, increased apoptosis, and reactive oxygen species (ROS) in LSCC cells. Mechanistically, ERCC6L promoted the binding of FOXM1 and KIF4A in LSCC cells, driving their progression. Targeting ERCC6L may provide a promising strategy for precision therapy in LSCC.