MicroRNA-625 inhibits cell invasion and epithelial-mesenchymal transition by targeting SOX4 in laryngeal squamous cell carcinoma

Laryngeal squamous cell carcinoma (LSCC) is a highly aggressive malignant cancer, but the molecular mechanisms underlying its development and progression remain largely elusive. The purpose of the present study is to investigate the expression profile and functional role of microRNA-625 (miR-625) in...

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Bibliographic Details
Published in:Bioscience reports 2019-01, Vol.39 (1)
Main Authors: Li, Yuan, Tao, Chenjuan, Dai, Lili, Cui, Caixia, Chen, Chaohui, Wu, Honglin, Wei, Qingyu, Zhou, Xuehua
Format: Article
Language:English
Subjects:
Aged
Carcinoma, Squamous Cell - genetics
Carcinoma, Squamous Cell - pathology
Cell Line, Tumor
Down-Regulation
Epithelial-Mesenchymal Transition - genetics
Female
Gene Expression Regulation, Neoplastic
Humans
Laryngeal Neoplasms - genetics
Laryngeal Neoplasms - pathology
Male
MicroRNAs - genetics
Middle Aged
SOXC Transcription Factors - genetics
SOXC Transcription Factors - metabolism
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Summary:Laryngeal squamous cell carcinoma (LSCC) is a highly aggressive malignant cancer, but the molecular mechanisms underlying its development and progression remain largely elusive. The purpose of the present study is to investigate the expression profile and functional role of microRNA-625 (miR-625) in LSCC. LSCC tissues and adjacent normal tissues were collected from 86 LSCC patients. The expression levels of miR-625 and SOX4 mRNA in tissues and cells were detected by RT-qPCR analysis. The expression levels of SOX4 and EMT-related proteins were detected by western blot analysis. cell proliferation, migration, and invasion were detected by MTT assay, colony formation assay, wound healing assay, and transwell invasion assay, respectively. Dual-luciferase reporter assay was performed to verify the binding relationship between miR-625 and the 3'-UTR of SOX4. The results demonstrated that miR-625 is significantly down-regulated in clinical LSCC tissues, and its low expression may be closely associated with unfavorable clinicopathological characteristics of LSCC patients. Overexpression of miR-625 significantly suppressed the proliferation, migration, invasion, and EMT of LSCC cells. Furthermore, SOX4 was validated as a direct target of miR-625 in LSCC cells, and rescue experiments suggested that restoration of SOX4 blocked the tumor suppressive role of miR-625 in LSCC cells. Taken together, these findings highlighted a critical role of miR-625 in the pathogenesis of LSCC, and restoration of miR-625 could be considered as a potential therapeutic strategy against this fatal disease.
ISSN:0144-8463
1573-4935
DOI:10.1042/BSR20181882