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通过下调CDCP1表达抑制miR-218对肺癌增殖或转移的作用。

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

作者信息

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

机构信息

Department of Cardiac Surgery, GuiZhou Province People's Hospital, Guiyang, China.

出版信息

Eur Rev Med Pharmacol Sci. 2017 Apr;21(7):1502-1508.

PMID:28429357
Abstract

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.

摘要

目的

肺癌是一种常见的恶性肿瘤,复发和转移风险高。非小细胞肺癌(NSCLC)是最常见的亚型。作为一种肿瘤生物标志物,微小RNA(miR)具有组织敏感性,可促进癌基因或抑制肿瘤抑制基因。MiR-218表达异常,可作为肿瘤的分子标志物之一。然而,其在肺癌细胞中的表达及作用机制尚未完全阐明。

材料与方法

检测体外培养的肺腺癌A549细胞和正常支气管上皮细胞系16HBE中miR-218的表达。用miR-218模拟物或阴性对照转染A549细胞,随后通过实时PCR定量检测miR-218。采用MTT法检测细胞增殖,同时采用Transwell小室检测细胞侵袭。采用双荧光素酶报告基因检测(DLRGA)检测miR-218与CDCP1之间的靶向关系。采用蛋白质免疫印迹法检测CDCP1的表达。

结果

与16HBE相比,A549细胞中miR-218表达下调(p<0.05)。转染miR-218模拟物显著促进miR-218表达,抑制肿瘤增殖或侵袭。作为miR-218的靶基因,miR-218过表达可抑制CDCP1的表达(与对照组相比,p<0.05)。

结论

MiR-218通过下调CDCP1抑制NSCLC的增殖或转移,可作为肺癌诊断的新型分子靶点。

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