OBJECTIVE: This study aimed at exploring the role and mechanism of Krüppel-like factor 5 (KLF5) in the migration, invasion, epithelial-mesenchymal transition (EMT) induction and proliferation in laryngeal cancer human epithelial type 2 (Hep-2) cells, and to provide a new sight for the treatment of laryngeal carcinoma.
MATERIALS AND METHODS: Hep-2 cells were randomly divided into three groups: control group (Control), KLF5 siRNA group (siKLF5) and control-siRNA group (NC). The effects of KLF5 inhibition on cell proliferation and apoptosis were assessed by 3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay and flow cytometer, respectively. Wound healing assay and transwell invasion experiments were used to determine cell migration and invasion. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot were used to compare the levels of KLF5, EMT-related genes E-cadherin, N-cadherin, Vimentin and Zinc finger transcription factors (Snail, Slug) expressions. The levels of nuclear transcription factor-κB (NF-κB-p65) and IκBα were also detected by Western blot.
RESULTS: Compared with the Control group, the proliferation rate of Hep-2 cells in the siKLF5 group was significantly decreased while the apoptosis rate was increased (p<0.05). Meanwhile, the migration and invasion ability of Hep-2 cells were markedly decreased (p<0.05). E-cadherin protein expression was up-regulated while Vimentin, N-cadherin, Snail, and Slug protein expression levels were downregulated in siKLF5 group (p<0.05). Silencing KLF5 could inhibit the expression of NF-κB phosphorylation at p65 and the IκBα degradation (p<0.05).
CONCLUSIONS: These results revealed that silencing KLF5 expression reduced the proliferation, migration and invasion and EMT abilities by inhibiting the NF-κB pathway in Hep-2 cells. Our results suggest that KLF5 may be a potential therapeutic target in laryngeal carcinoma.
To cite this article
F.-F. Liu, L. Dong, X. Yang, D.-J. Li, Y.-Y. Shen, Z.-L. Liu
KLF5 silence attenuates proliferation and epithelial-mesenchymal transition induction in Hep-2 cells through NF-κB signaling pathway
Eur Rev Med Pharmacol Sci
Vol. 23 - N. 9