Rong Wang

Department of Oncology, the First Affiliated Hospitalof Nanjing Medical University

Objective:MicroRNA plays a crucial role indevelopment and progression of multiple malignancies. However, the mechanismsof microRNA in cancer are not totally clear. To verify our hypothesis thatmiR-326 regulates cell proliferation and migration in lung cancer by targetingPhox2a and is regulated by HOTAIR. Method: Lung cancer cell lines A549and H838, nude mice with lung cancer xenograft and lung cancer tissue samplesare used. we investigate effects of miR-326 on cell proliferation, migration,cell cycle and apoptosis in lung cancer. Real time PCR, western blot,adenovirus, RNA interference, luciferase assays are employed toinvestigate molecular mechanisms of HOTAIR/miR-326/Phox2a regulation pathway inlung cancer. Result: Our data showed enforced expression of miR-326inhibited cell proliferation and migration in vitro and tumor growth in nudemice, decreased proportion of cells in S phase and increased cell apoptosis inboth A549 and H838 cells. In addition, we found miR-326 bound to 3'UTR of Phox2abut not KLF3 and enforced expression of miR-326 decreased accumulation ofPhox2a in both A549 and H838. Moreover, exogenous expression of Phox2acompromised inhibitory effects of miR-326 on cell proliferation and migration.We also found silencing of HOTAIR caused increased expression of miR-326. Conclusion:In conclusion, HOTAIR, miR-326 and Phox2a communicates with each other andcomprise a miR-326-based regulation network, which is crucial forproliferation, metastasis and invasion of lung cancer. Our project will providenew information for lung cancer development and progression, and help establishnovel strategy for lung cancer diagnosis and therapy.

Key Words: miR-326  lung cancer cell proliferation and migrate