M Xia1, M-L Duan, J-H Tong, J-G Xu. 1. Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China. sys80860149@sina.com.
Abstract
OBJECTIVE: Lung cancer, including non-small cell lung cancer (NSCLC), is the leading cause of cancer-related mortality worldwide. Despite recent advances in clinical and experimental oncology, the prognosis of patients with NSCLC still remains poor and the average survival time of patients suffer from lung cancer is low. Therefore, the potential mechanism accounting for the tumorigenesis of NSCLC is still needed to be explored. MATERIALS AND METHODS: A lentiviral vector over-expressing miR-26b in A549 lung cancer cells was constructed. Cell proliferation, migration and invasion analysis were measured by cell counting kit (MTT), would healing assay and Transwell assay. Direct target of miR-26b in A549 cells was examined using bioinformatics and Luciferase assay. RESULTS: Herein, we found that over-expression of miR-26b significantly inhibited the proliferation, migration and invasion of A549 lung cancer cell in vitro and suppressed the growth of established tumors in vivo. By using bioinformatics, we found that COX-2 (Cyclooxygenase-2) is one of the potential targets of miR-26b. Moreover, miR-26b was found to negatively regulate COX-2 protein level by directly targeting its 3'UTR. In addition, depletion of endogenous COX-2 by the specific siRNA could mimic the function of miR-26b overexpression. CONCLUSIONS: Taken together, our results demonstrate that miR-26b could suppress lung cancer cells proliferation, migration and invasion by directly negative regulation of COX-2. MiR-26b could serve as a novel potential marker for NSCLC therapy.
OBJECTIVE:Lung cancer, including non-small cell lung cancer (NSCLC), is the leading cause of cancer-related mortality worldwide. Despite recent advances in clinical and experimental oncology, the prognosis of patients with NSCLC still remains poor and the average survival time of patients suffer from lung cancer is low. Therefore, the potential mechanism accounting for the tumorigenesis of NSCLC is still needed to be explored. MATERIALS AND METHODS: A lentiviral vector over-expressing miR-26b in A549 lung cancer cells was constructed. Cell proliferation, migration and invasion analysis were measured by cell counting kit (MTT), would healing assay and Transwell assay. Direct target of miR-26b in A549 cells was examined using bioinformatics and Luciferase assay. RESULTS: Herein, we found that over-expression of miR-26b significantly inhibited the proliferation, migration and invasion of A549 lung cancer cell in vitro and suppressed the growth of established tumors in vivo. By using bioinformatics, we found that COX-2 (Cyclooxygenase-2) is one of the potential targets of miR-26b. Moreover, miR-26b was found to negatively regulate COX-2 protein level by directly targeting its 3'UTR. In addition, depletion of endogenous COX-2 by the specific siRNA could mimic the function of miR-26b overexpression. CONCLUSIONS: Taken together, our results demonstrate that miR-26b could suppress lung cancer cells proliferation, migration and invasion by directly negative regulation of COX-2. MiR-26b could serve as a novel potential marker for NSCLC therapy.