MicroRNA-30d inhibits the migration and invasion of human esophageal squamous cell carcinoma cells via the post-transcriptional regulation of enhancer of zeste homolog 2

Autor: Tian-Heng Ma, Hong-Gang Wang, Shang-Nong Wu, Wei Yan, Cheng-Cheng Gao, Rui Xie, Xiao-Zhong Yang, Jia-Ling Zhang
Rok vydání: 2017
Předmět:
Male
0301 basic medicine
Cancer Research
Esophageal Neoplasms
Blotting
Western
Cell
Biology
Real-Time Polymerase Chain Reaction
03 medical and health sciences
Esophagus
0302 clinical medicine
Cell Movement
microRNA
Biomarkers
Tumor
Tumor Cells
Cultured
medicine
Humans
Enhancer of Zeste Homolog 2 Protein
Neoplasm Invasiveness
RNA
Messenger
Cell Proliferation
Neoplasm Staging
Regulation of gene expression
Oncogene
Reverse Transcriptase Polymerase Chain Reaction
Cell growth
EZH2
General Medicine
Middle Aged
Cell cycle
Prognosis
Molecular biology
digestive system diseases
Gene Expression Regulation
Neoplastic
MicroRNAs
030104 developmental biology
medicine.anatomical_structure
Oncology
Case-Control Studies
Lymphatic Metastasis
030220 oncology & carcinogenesis
Cancer cell
Carcinoma
Squamous Cell
Female
Zdroj: Oncology Reports. 37:1682-1690
ISSN: 1791-2431
1021-335X
DOI: 10.3892/or.2017.5405
Popis: The present study was carried out to investigate the expression pattern, clinical significance and biological functions of microRNA-30d (miR-30d) in esophageal carcinogenesis. Quantitative real-time PCR was performed to detect the expression levels of miR-30d in esophageal squamous cell carcinoma (ESCC) tissues and cell lines. Then, associations between miR-30d expression and various clinicopathological features of patients with ESCC were statistically evaluated. In addition, the effects of miR-30d on the migration and invasion of two human ESCC cell lines transfected with miRNA or co-transfected with miRNA mimics and the expression vector of its target gene were determined. The results revealed that the expression levels of miR-30d were markedly decreased in ESCC tissues and cell lines, comparing with the corresponding normal controls. Notably, reduced expression of miR-30d occurred more frequently in ESCC patients with positive lymph node metastasis, moderate-poor differentiation and advanced tumor-node-metastasis stage than those with negative features. Functionally, enforced expression of miR-30d was found to inhibit cell invasion and migration of the ESCC cell lines. Luciferase reporter assay identified enhancer of zeste homolog 2 (EZH2) as a direct target gene of miR-30d. The expression level of EZH2 mRNA was negatively correlated with the expression of miR-30d in the ESCC tissues. Moreover, the inhibitory effect of miR-30d on ESCC cell motility was reversed by EZH2 overexpression. Collectively, these findings provide convincing evidence that decreased expression of miR-30d may be implicated in esophageal carcinogenesis and progression. We also confirmed miR-30d as a tumor-suppressor which may inhibit cancer cell motility by targeting EZH2, a potential therapeutic target for ESCC.
Databáze: OpenAIRE
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