Inhibition of pulmonary carcinoma proliferation or metastasis of miR-218 via down-regulating CDCP1 expression

X.-J. Zeng, Y.-H. Wu, M. Luo, P.-G. Cong, H. Yu

Department of Cardiac Surgery, GuiZhou Province People’s Hospital, Guiyang, China. xiangjunzeng07@163.com

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• Oncology

OBJECTIVE: Pulmonary carcinoma is one common malignant tumor with a high risk of recurrence and metastasis. Non-small cell lung cancer (NSCLC) is the most common subtype. As one tumor biomarker, microRNA (miR) has tissue sensitivity and can facilitate oncogene or inhibit tumor suppressor gene. MiR-218 has abnormal expression and can work as one molecular marker for tumors. However, its expression and function mechanism in lung cancer cells have not been fully illustrated.

MATERIALS AND METHODS: In vitro cultured pulmonary adenoma A549 cells and normal bronchial epithelial cell line 16HBE were tested for miR-218 expression. A549 cells were transfected with miR-218 mimic or negative controls, followed by real-time PCR quantifying for miR-218. MTT method was used to test cell proliferation, whilst Transwell chamber was adopted for measuring cell invasion. Dual luciferase reporter gene assay (DLRGA) was used to test target relationship between miR-218 and CDCP1. Western blot was used to test CDCP1 expression.

RESULTS: MiR-218 was down-regulated in A549 cells compared to 16HBE (p<0.05). Transfection of miR-218 mimic significantly facilitated miR-218 expression, inhibited tumor proliferation or invasion. As the target gene of miR-218, CDCP1 expression was suppressed by miR-218 over-expression (p<0.05 compared to control group).

CONCLUSIONS: MiR-218 inhibits NSCLC proliferation or metastasis via down-regulating CDCP1, and can work as one novel molecular target for lung cancer diagnosis.

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