Open AccessMiR‑148a modulates HLA‑G expression and influences tumor apoptosis in esophageal squamous cell carcinoma
Author(s) -
Quan Chen,
Guanghua Luo,
Xiaoying Zhang
Publication year - 2017
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2017.5058
Subject(s) - oncogene , apoptosis , molecular medicine , cell cycle , cancer research , esophageal squamous cell carcinoma , cell , biology , esophageal cancer , basal cell , cancer , carcinoma , medicine , pathology , biochemistry , genetics
Esophageal cancer (EC) is a common malignant tumor type, and esophageal squamous cell carcinoma (ESCC) accounts for the majority of EC cases. Previous studies have reported that microRNA (miR)-148a is downregulated in patients with recurrent EC. The human leukocyte antigen-G (HLA-G) is expressed to a high level in primary ESCC tissues and is associated with prognosis. A previous luciferase assay indicated that HLA-G is a target of miR-148a regulation. The aim of the current study was to investigate the expression level of miR-148a in primary ESCC. The regulatory role of miR-148a in HLA-G expression and cell proliferation in ESCC cells was also investigated. The relative expression level of miR-148a was compared between ESCC tumor tissues and adjacent normal tissues. The human ESCC cell line EC9706 was transfected with miR-148a mimic, non-homologous RNA duplex (negative control; NC) or empty vector (blank control; BC). Reverse transcription-quantitative polymerase chain reaction and western blot analysis were used to assess the level of HLA-G expression. The cells were stained with Annexin V-fluorescein isothiocyanate/propidium iodide and cell apoptosis was evaluated by flow cytometry. The level of miR-148a expression was significantly lower in primary ESCC tissues compared with adjacent normal tissues (P<0.01). In EC9706 cells transfected with miR-148a mimic, the rate of apoptosis was increased ~13-fold when compared with BC cells (P<0.01). Furthermore, the mRNA level of HLA-G was significantly reduced in cells transfected with miR-148a mimic (P<0.01). The protein levels of HLA-G were also notably decreased. Transfection with non-homologous RNA duplex did not influence the rate of cell apoptosis or expression of HLA-G when compared with the BC group. In conclusion, miR-148a was indicated to be involved in carcinogenesis in primary ESCC through the regulation of HLA-G expression. The current results suggest that miR-148a is a potential biomarker of ESCC.