The inhibition of KLF6 suppresses the proliferation of nasopharyngeal carcinoma cells and promotes apoptosis by inducing cell cycle arrest

Abstract

To investigate the role of KLF6 in nasopharyngeal carcinoma (NPC) cells. NPC C666-1 cells were transfected with si-NC, si-KLF6, miR-181-5p mimics, and miR-NC. The transfection efficiency was evaluated using qRT-PCR to measure the expression of miR-181-5p and KLF6. The protein expression level of KLF6 was detected using WB assay. Cell proliferation was assessed using the CCK8 assay to determine the effect of KLF6. Flow cytometry was used to detect apoptosis and changes in the cell cycle of NPC cells after KLF6 inhibition. The targeting relationship between miR-181-5p and KLF6 was verified using dual fluorescein assay. The qRT-PCR results demonstrated successful transfection of si-NC, si-KLF6, miR-181-5p mimics, and miR-NC. Inhibition of KLF6 led to a decrease in miR-181 expression, whereas overexpression of miR-181-5p increased KLF6 expression. Furthermore, suppressing KLF6 expression resulted in inhibited proliferation of C666-1 cells and enhanced apoptosis. This led to an increase in S-phase cells and a decrease in G₂/M-phase cells. The dual luciferase results confirmed the targeted binding between miR-181-5p and KLF6. Inhibition of KLF6 suppresses NPC cell proliferation and promotes apoptosis through induction of cell cycle arrest.