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1.
Int J Clin Exp Pathol ; 8(11): 14983-8, 2015.
Article in English | MEDLINE | ID: mdl-26823832

ABSTRACT

OBJECTIVE: MiRNAs play crucial roles in progression of cancer. However, the underlying mechanisms of miRNAs in non small cell lung cancer are still poorly understood. The aim of this study was to investigate the expression level of microRNA-126 (miR-126) and microRNA-133b (miR-133b) and also their association with clinicopathological features in patients with non small cell lung cancer (NSCLC). METHODS: Total RNA was purified from NSCLC tissues and adjacent non-tumor tissues and then quantitative real-time PCR (qRT-PCR) was used to evaluate the expression rate of microRNAs. Furthermore, the association of miR-126 and miR-133b level with clinicopathological features and prognosis were evaluated. RESULTS: Our findings showed that expression of miR-126 was decreased in NSCLC tissues compared with adjacent non-tumor tissues. On the other hand, a lower expression of miR-133b was seen in NSCLC tissues when compared with adjacent non-tumor tissues. In term of miR-126, our results showed that miR-126 was associated with tumor stage and lymph nodes metastasis (P<0.05). In term of miR-133b, our finding indicated that decreased expression of miR-133b was correlated with advanced tumor stage and lymph nodes metastasis (P<0.05). Kaplan-Meier analysis and log-rank test indicated that patients with low expression of miR-126 and miR-133b had a shorter overall survival (log-rank test; P<0.05). Multivariate Cox proportional hazards model revealed that low expression of miR-126 and miR-133b, advanced tumor stage and lymph nodes metastasis were independent prognostic factors for overall survival of NSCLC patients. CONCLUSIONS: These findings suggested that miR-126 and miR-133b might play a key role in the progression and metastasis of NSCLC and would be applied as a novel therapeutic agent.


Subject(s)
Biomarkers, Tumor/analysis , Carcinoma, Non-Small-Cell Lung/pathology , Lung Neoplasms/pathology , Adult , Aged , Carcinoma, Non-Small-Cell Lung/genetics , Carcinoma, Non-Small-Cell Lung/mortality , Disease Progression , Disease-Free Survival , Down-Regulation , Female , Humans , Kaplan-Meier Estimate , Lung Neoplasms/genetics , Lung Neoplasms/mortality , Lymphatic Metastasis/genetics , Lymphatic Metastasis/pathology , Male , MicroRNAs , Middle Aged , Prognosis , Proportional Hazards Models , Real-Time Polymerase Chain Reaction
2.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue ; 20(2): 69-71, 2008 Feb.
Article in Chinese | MEDLINE | ID: mdl-18279586

ABSTRACT

OBJECTIVE: To investigate the expression of scavenger receptor class A (SR-A) in lung tissue and alveolar macrophage (AM) in mice with acute lung injury (ALI) induced by lipopolysaccharide (LPS). METHODS: The model of ALI was reproduced by intraperitoneal (ip) injection of LPS (5 mg/kg), and the expression of SR-A was observed in lung tissue and AM, and the expression and distribution of J774 A.1 were also studied by using mouse macrophage line. RESULTS: Partial pressure of oxygen in artery (PaO(2)) of lung tissue in LPS groups was significantly lower while wet/dry weight (W/D) ratio was higher than those in normal saline control group (both P<0.01). SR-A was widely expressed in murine lung, including AM, pulmonary vascular endothelial cells, vascular smooth muscle cells, lung epithelial cells and polymorphonuclear neutrophils. Immunohistochemical staining showed that, during the course of development of ALI in mice, the expression of SR-A was gradually down-regulated with the elapse of time after ip injection of LPS, The same result was seen in the isolated AM, and especially marked in group 4 hours and group 8 hours. In vitro, the expression of SR-A on J774 A.1 cells decreased was also down-regulated when treated with LPS. CONCLUSION: SR-A was widely expressed in murine lung. During the course of ALI, the expression of SR-A in the murine lung and AM is down-regulated, which may be induced by LPS.


Subject(s)
Acute Lung Injury/metabolism , Lipopolysaccharides/toxicity , Lung/metabolism , Scavenger Receptors, Class A/metabolism , Animals , Disease Models, Animal , Female , Macrophages, Alveolar/metabolism , Male , Mice , Random Allocation
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