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18 November 2015 : Laboratory Research

Effect of miR-503 Down-Regulation on Growth and Invasion of Esophagus Carcinoma and Related Immune Function

Ke ZhaoBC, Bao-Jun ChenAD, Zhi-Guo ChenFG, Yong-Jian ZhangCE, Di XuBF, Qi LiuAG

DOI: 10.12659/MSM.895518

Med Sci Monit 2015; 21:3564-3569

Abstract

BACKGROUND: MicroRNA (miR) has been proved to be an important biomarker for tumors because it can regulate occurrence, progression, invasion, and metastasis of cancer. A previous study has shown the involvement of miR-503 in multiple gastrointestinal tumors. Its detailed role and immune regulatory function in esophagus carcinoma, however, remains unknown. This study thus investigated the effect of miR-503 in regulating growth, proliferation, and invasion of esophagus cancer and its influence on cytokine secretion.

MATERIAL AND METHODS: Esophagus carcinoma cell line EC9706 and normal esophageal epithelial cell line HEEC were transfected with miR-503 inhibitor. MTT assay was used to quantify the cell proliferation, and a Transwell chamber was used to evaluate cell invasion. Release of cytokines, including interleukin-2 (IL-2), IL-4, IL-10, and interferon-γ (IFN-γ), was measured by enzyme-linked immunosorbent assay (ELISA).

RESULTS: MiR-503 expression was significantly elevated in esophagus carcinoma cells (p<0.05). The specific inhibition of miR-503 expression remarkably suppressed proliferation and invasion of tumor cells. It can also down-regulated IL-2 and IFN-γ expression and facilitate secretion of IL-4 and IL-10 when compared to the control group (p<0.05 in all ceases).

CONCLUSIONS: The inhibition of miR-503 can effectively inhibit tumor progression and improve immune function, suggesting its potency as a novel drug target for esophagus cancer treatment.

Keywords: Case-Control Studies, Carcinoma, Acinar Cell - genetics, Cell Proliferation - drug effects, Cytokines - metabolism, Down-Regulation - drug effects, Esophageal Neoplasms - therapy, Interferon-gamma - metabolism, Interleukins - metabolism, Oligonucleotides - genetics, Random Allocation, Tumor Necrosis Factor Ligand Superfamily Member 13 - metabolism

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750