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Micro RNA ‐26a inhibits proliferation and tumorigenesis via targeting CKS 2 in laryngeal squamous cell carcinoma
Author(s) -
Wu Zhiyan,
Lu Baocai,
Li Xiao,
Miao Wenjie,
Li Jin,
Shi Yongjuan,
Yu Wenfa
Publication year - 2018
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12890
Subject(s) - cell growth , carcinogenesis , cancer research , in vivo , cell , gentamicin protection assay , luciferase , chemistry , cell culture , cell migration , reporter gene , microbiology and biotechnology , nude mouse , biology , gene expression , transfection , western blot , gene , biochemistry , genetics
Summary Laryngeal squamous cell carcinoma ( LSCC ) is one of the most common head and neck cancers, with high mortality and incidence. Micro RNA ‐26a (miR‐26a) is involved in the development and progression of several tumours. However, the roles of miR‐26a and its target CKS 2 in LSCC progression are not yet clear. The mRNA and protein expression was determined using RT ‐ PCR and Western blotting assay, respectively. Cell proliferation was detected using a Cell Counting kit‐8 assay ( CCK ‐8). Transwell assay was used to evaluate cell migration and invasion. Dual‐luciferase reporter assay was applied to determine the relationship between miR‐26a and CKS 2. In addition, a tumour xenograft model in nude mice was established to further determine the effects of miR‐26a on tumourigenesis. In this study, we found that miR‐26a level was down‐regulated in LSCC tissues and cell lines, while CKS 2 expression was increased. Cell proliferation, migration, invasion and the expression of MMP 2 and MMP 9 was suppressed by miR‐26a overexpression, but enhanced by inhibition of miR‐26a. Dual‐luciferase reporter assay demonstrated that CKS 2 is a direct target of miR‐26a in AMC ‐ HN ‐8 cells. Overexpression of miR‐26a caused a significant reduction in CKS 2 expression, and reinforced expression of CKS 2 abolished the tumour‐suppressive function of miR‐26a. Moreover, miR‐26a inhibited tumour growth in vivo. Taken together, miR‐26a inhibited proliferation and tumourigenesis of LSCC via targeting CKS 2 in vitro and in vivo.