Open AccessMiR ‐32‐5p promoted epithelial‐to‐mesenchymal transition of oral squamous cell carcinoma cells via regulating the KLF2 / CXCR4 pathway
Author(s) -
Qin ShiYu,
Li Bo,
Chen Mei,
Qin MingQun,
Liu JiMu,
Lv QiuLi
Publication year - 2022
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1002/kjm2.12450
Subject(s) - medicine , cxcr4 , epithelial–mesenchymal transition , klf2 , cancer research , metastasis , cancer , downregulation and upregulation , biochemistry , gene , receptor , chemokine , chemistry
Abstract Oral squamous cell carcinoma (OSCC) is one of the most common carcinomas of the oral cavity. However, the regulatory mechanisms on miR‐32‐5p remain poorly understood in OSCC. The expression of miR‐32‐5p, Krüppel‐like factor 2 (KLF2), C‐X‐C motif chemokine receptor 4 (CXCR4), and epithelial‐to‐mesenchymal transition (EMT)‐related proteins (E‐cadherin, Vimentin, N‐cadherin, and Snail) were evaluated were assessed using RT‐qPCR and Western blot. 3‐(4, 5‐Dimethylthiazolyl2 )‐2, 5‐diphenyltetrazolium bromide assay, wound healing assay, and transwell assay were employed to detect cell proliferation, migration, and invasion of OSCC cells. Finally, dual‐luciferase reporter assay was performed to verify the binding relationship between KLF2 and miR‐32‐5p. MiR‐32‐5p was highly expressed while KLF2 was lowly expressed in OSCC cells, and miR‐32‐5p knockdown or KLF2 overexpression could markedly reduce cell proliferation, migration, invasion, and EMT of OSCC cells. What is more, KLF2 was the target of miR‐32‐5p, and knockdown of KLF2 abolished the inhibitory effect of miR‐32‐5p inhibitor on progression of OSCC. Finally, CXCR4 expression was negatively regulated by KLF2, and inhibition of CXCR4 obviously alleviated the biological effects of si‐KLF2 on the progression of OSCC. MiR‐32‐5p could enhance cell proliferation, migration, invasion, and EMT of OSCC cells, and the discovery of miR‐32‐5p/KLF2/CXCR4 axis might provide potential therapeutic targets for OSCC.