Yanhong Shang1, Aimin Zang1, Jinghua Li2, Youchao Jia1, Xiaofang Li1, Lei Zhang1, Ran Huo1, Jihong Yang3, Jia Feng1, Kun Ge4, Yongbin Yang5, Yan Zhang6, Jing Jiang7. 1. Hebei Key Laboratory of Cancer Radiotherapy and Chemotherapy, Department of Medical Oncology, Affiliated Hospital of Hebei University, Baoding, 071000, China. 2. Department of General Surgery, Affiliated Hospital of Hebei University, Baoding, 071000, China. Electronic address: zch7881@aol.com. 3. Department of General Surgery, Affiliated Hospital of Hebei University, Baoding, 071000, China. 4. Department of Science and Research, Affiliated Hospital of Hebei University, Baoding, 071000, China. 5. Department of Pathology, Health Science Center, Hebei University, Baoding, 071000, China. 6. Department of Medical Oncology, The First Hospital of ShiJiazhuang, ShiJiazhuang, 050010, China. 7. Department of Clinical Epidemiology, The First Hospital of Jilin University, Changchun, 130021, China.
Abstract
PURPOSE: The purpose of this study is to examine the expression and clinical significance microRNA-383 (miR-383) in non-small cell lung cancer (NSCLC) both in vitro and in vivo. METHODS: Tumorous miR-383 expressions were compared between NSCLC cell lines and normal lung cells. MiR-383 was upregulated in A549 and H596 cells to evaluate its tumor suppressive effect on NSCLC proliferation, invasion and migration in vitro. MiR-383 expression was also compared between 139-paired clinical NSCLC tissues and their adjacent non-carcinoma lung tissues, as well as between early-stage NSCLC tissues and advanced-stage NSCLC tissues. Correlation between tumorous miR-383 expression and NSCLC patients' clinicopathological features and overall survival (OS) were also statistically analyzed. RESULTS: MiR-383 was significantly downregulated in NSCLC cell lines. MiR-383 overexpression reduced proliferation, invasion and migration of A549 and H596 cells. In clinical samples, miR-383 was also found to be markedly downregulated in NSCLC carcinomas than in non-carcinoma lung tissues, and in advanced-stage carcinomas than in early-stage carcinomas. It was also found low tumorous miR-383 expression was significantly associated with NSCLC patients' poor prognosis, including advanced TNM stages, positive lymph node metastasis, and shorter OS. CONCLUSION: Endogenous miR-383 is a functional tumor suppressor in NSCLC. It may also serve as an independent prognostic factor for patients with NSCLC.
PURPOSE: The purpose of this study is to examine the expression and clinical significance microRNA-383 (miR-383) in non-small cell lung cancer (NSCLC) both in vitro and in vivo. METHODS:TumorousmiR-383 expressions were compared between NSCLC cell lines and normal lung cells. MiR-383 was upregulated in A549 and H596 cells to evaluate its tumor suppressive effect on NSCLC proliferation, invasion and migration in vitro. MiR-383 expression was also compared between 139-paired clinicalNSCLC tissues and their adjacent non-carcinoma lung tissues, as well as between early-stage NSCLC tissues and advanced-stage NSCLC tissues. Correlation between tumorousmiR-383 expression and NSCLCpatients' clinicopathological features and overall survival (OS) were also statistically analyzed. RESULTS:MiR-383 was significantly downregulated in NSCLC cell lines. MiR-383 overexpression reduced proliferation, invasion and migration of A549 and H596 cells. In clinical samples, miR-383 was also found to be markedly downregulated in NSCLC carcinomas than in non-carcinoma lung tissues, and in advanced-stage carcinomas than in early-stage carcinomas. It was also found low tumorousmiR-383 expression was significantly associated with NSCLCpatients' poor prognosis, including advanced TNM stages, positive lymph node metastasis, and shorter OS. CONCLUSION: Endogenous miR-383 is a functional tumor suppressor in NSCLC. It may also serve as an independent prognostic factor for patients with NSCLC.
Authors: Sassine Ghanem; Sandy El Bitar; Sami Hossri; Chanudi Weerasinghe; Jean Paul Atallah Journal: Cancer Manag Res Date: 2017-07-06 Impact factor: 3.989