Peng Xiao1, Wen-Liang Liu2. 1. Department of Thoracic Surgery, The Third Xiangya Hospital, Central South University No 138 Tong-Zipo Road, Changsha 410013, Hunan Province, P. R. China. 2. Department of Thoracic Surgery, The Second Xiangya Hospital, Central South University No 139 Ren-Min Middle Road, Changsha 410011, Hunan Province, P. R. China.
Abstract
BACKGROUND: microRNAs (miRNAs) play a significant role in cancer development and progression by regulating the expression of oncogenes or tumor suppressor genes. Previous study using microarrays demonstrated that miR-142-3p was downregulated in patients with Non-small-cell lung carcinoma (NSCLC). However, the functional role of miR-142-3p in NSCLC is still unclear. MATERIAL AND METHOD: Real-time quantitative PCR was applied to evaluate the expression level of miRNA-142-3p in NSCLC and normal samples. The cell proliferation of NSCLC cells was analyzed by MTT and colony formation assay after miR-142-3p transfection. Luciferase activities assay, cotransfection and Western blot were used to reveal that the predicted target genes of miR-125b were direct and specific. RESULTS: In this study, we demonstrate miR-142-3p was downregulated in NSCLC tissues and cell lines. We demonstrated that the overexpression of miR-142-3p inhibits NSCLC cell proliferation and induced cell apoptosis. Furthermore, we demonstrate HMGB1 was a directly target of miR-142-3p in NSCLC cells, and confirmed the target specificity between miR-142-3p and the HMGB1 3'-untranslated region by luciferase reporter assay. CONCLUSIONS: These results suggest that miR-142-3p may be a tumor suppressor through the downregulation of HMGB1 in NSCLC. miR-142-3p may be a tumor suppressor and a potential therapeutic agent for patients with NSCLC.
BACKGROUND: microRNAs (miRNAs) play a significant role in cancer development and progression by regulating the expression of oncogenes or tumor suppressor genes. Previous study using microarrays demonstrated that miR-142-3p was downregulated in patients with Non-small-cell lung carcinoma (NSCLC). However, the functional role of miR-142-3p in NSCLC is still unclear. MATERIAL AND METHOD: Real-time quantitative PCR was applied to evaluate the expression level of miRNA-142-3p in NSCLC and normal samples. The cell proliferation of NSCLC cells was analyzed by MTT and colony formation assay after miR-142-3p transfection. Luciferase activities assay, cotransfection and Western blot were used to reveal that the predicted target genes of miR-125b were direct and specific. RESULTS: In this study, we demonstrate miR-142-3p was downregulated in NSCLC tissues and cell lines. We demonstrated that the overexpression of miR-142-3p inhibits NSCLC cell proliferation and induced cell apoptosis. Furthermore, we demonstrate HMGB1 was a directly target of miR-142-3p in NSCLC cells, and confirmed the target specificity between miR-142-3p and the HMGB1 3'-untranslated region by luciferase reporter assay. CONCLUSIONS: These results suggest that miR-142-3p may be a tumor suppressor through the downregulation of HMGB1 in NSCLC. miR-142-3p may be a tumor suppressor and a potential therapeutic agent for patients with NSCLC.
Authors: A M Flohr; P Rogalla; M Meiboom; L Borrmann; M Krohn; B Thode-Halle; J Bullerdiek Journal: Anticancer Res Date: 2001 Nov-Dec Impact factor: 2.480
Authors: H Rauvala; H J Huttunen; C Fages; M Kaksonen; T Kinnunen; S Imai; E Raulo; I Kilpeläinen Journal: Matrix Biol Date: 2000-09 Impact factor: 11.583