Background: Laryngeal cancer (LCA) is a common head and neck cancer. Lysine demethylase 5B (KDM5B ) knockdown is expected as a new target for cancer prevention. We investigated the molecular mechanism of KDM5B  in LCA.
Materials and Methods: The levels of KDM5B , microRNA (miR)-139-3p  and high-mobility-group box 2 (SOX2 ) in LCA tissues and cells, normal tissues and cells were detected. The effect of KDM5B  on LCA was evaluated. The upstream miR of KDM5B  and the downstream gene and pathway of KDM5B  were predicted and their effects on LCA were analyzed. The Wnt/β-catenin pathway-specific activator agonist was delivered into LCA cells expressing miR-139-3p  mimic to evaluate the role of the Wnt/β-catenin pathway.
Results: KDM5B  was highly expressed in LCA, and inhibition of KDM5B  suppressed LCA progression. miR-139-3p , downregulated in LCA tissues, was a regulatory miR of KDM5B . Overexpression of miR-139-3p  significantly inhibited the malignant biological behaviors of LCA cells. KDM5B  promoted SOX2  expression via histone demethylation. SOX2  was highly expressed in LCA, and overexpression of SOX2  promoted LCA progression by inducing the Wnt/β-catenin pathway. Activated Wnt/β-catenin pathway attenuated the inhibitory effect of miR-139-3p  mimic on the malignant biological behaviors of LCA cells.
Conclusion: miR-139-3p  overexpression inhibited LCA development via regulating the KDM5B/SOX2 axis and inhibiting the Wnt/β-catenin pathway.
Keywords: laryngeal cancer, microRNA-139-3p , lysine demethylase 5B, high-mobility-group box 2, Wnt/β-catenin pathway