Abstract

ObjectionThe aim of this study is to explain the significance and mechanism of miR-205 in the diagnosis and treatment of non-small cell lung cancer. MethodsThe 70 advanced NSCLC patients, treated in our hospital, were collected from 2011.10 to 2013.9, taking the tissues from cancer and adjacent tissues to measure the miR-205 expression, evaluate the AKT gene and protein expression of cancer and adjacent normal tissues by RT-PCR and Immunohistochemistry (IHC) assays and analyzing the correlation between miR-205 and AKT. Following up the patients for 2 years; Recording patients’ survival time. In the cell experiment, Selecting A549 cell as research object, the cells were divided into three groups: Normal control group (NC), Blank control group (BL) and si-miR-205 transfection group (si-miR-205). Cell proliferation rate and apoptosis rate were detected by MTT method and flow cytometry; Measuring invasion and migration of difference groups by transwell and scratch testing, measured the Akt, mTOR,P21, MMP2 and MMP9 gene expression and detected Akt, p-Akt, mTOR, p-mTOR, P21, MMP2 and MMP 9 protein expression levels. ResultsCompared with adjacent normal tissue, the miR-205 and AKT gene expression level was significantly increased in NSCLC tissues (P<0.05) and the AKT protein expression was stronger than that of healthy tissues, miR-205 was positive correlation with AKT; In the overall survival, MiR-205 high expression group was significantly higher than low expression group (P<0.05). In the cell experiment, Compared with NC and BL groups, si-miR-205 could significantly reduced the biological activity of A549 cells in proliferation, invasion and migration, and promoted the apoptosis of A549 cells (P<0.05, respectively). Akt, p-Akt, mTOR, p-mTOR, P21, MMP 2 and MMP 9 gene and protein expression of si-miR-205 group were significantly compared with NC and BL groups (P<0.05, respectively). ConclusionmiRNA-205 might serve as a potential biomarker for the prognosis of advanced NSCLC, and inhibiting miR-205 expression could decrease A549 cells biological activity by regulating Akt/mTOR/P21 and Akt/MMP 2/MMP 9signaling pathway.

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