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Ke Zhao, Bao-Jun Chen, Zhi-Guo Chen, Yong-Jian Zhang, Di Xu, Qi Liu
(Department of Thoracic Surgery, The Central Hospital of Wuhan, Wuhan, Hubei, China (mainland))
Med Sci Monit 2015; 21:3564-3569
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: Cell Line, Tumor, Case-Control Studies, Carcinoma, Acinar Cell - genetics, Cell Proliferation - drug effects, Cytokines - metabolism, Down-Regulation - drug effects, Esophageal Neoplasms - therapy, Gene Expression Regulation, Neoplastic, Interferon-gamma - metabolism, Interleukins - metabolism, MicroRNAs - metabolism, Oligonucleotides - genetics, Random Allocation, Tumor Necrosis Factor Ligand Superfamily Member 13 - metabolism