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    Circular RNA PVT1 acts as a competing endogenous RNA for miR-497 in promoting non-small cell lung cancer progression 
    Si Qina,1, Yue Zhaoa,1, Gwanyong Limb, Hongjing Lina, Xueli Zhanga, Xiaohong Zhanga,
    a Department of Respiration, The First Hospital of Jilin University, No. 71 Xinmin Street, Changchun, 130021, Jilin Province, China
    b Shenzhen College of International Education, First HuangGang Park Street, Shenzhen 518048, Guangdong Province, China
    Non-small cell lung cancer
    Circular RNA PVT1
    Competing endogenous RNA 
    Circular RNAs (circRNAs) are a class of covalently closed non-coding RNAs and play crucial regulatory roles in human cancer biology. The purpose of the present study was to explore the expression pattern and biological role of circular RNA PVT1 (circPVT1) in non-small cell lung cancer (NSCLC). We firstly found that circPVT1 was overexpressed in clinical NSCLC tissues and cell lines. NSCLC patients with high expression of circPVT1 ex-hibited aggressive clinicopathological characteristics and poor prognosis. In vitro assays of the NSCLC cell lines (H1299 and A549 cells) demonstrated that knockdown of circPVT1 inhibited NSCLC cell proliferation and in-duced NSCLC cell apoptosis. We further found that circPVT1 served as a competing endogenous RNA of miR-497 and indirectly regulated Bcl-2 expression in NSCLC cells. Finally, inhibition of miR-497 abrogated the effects of circPVT1 knockdown in NSCLC cells. Taken together, the results from our study indicated circPVT1 acts as an oncogene in NSCLC, and may serve as a promising therapeutic target for NSCLC patients.
    1. Introduction
    Lung cancer is one of the most common causes of GW311616 cancer-related death both in men and women worldwide [1], and among all lung cancer patients, about 85% of patients are diagnosed with non-small cell lung cancer (NSCLC) [2]. Many NSCLC patients are diagnosed at an advanced stage. Unfortunately, despite the great advances in ther-apeutic technique over the past few decades, the 5-year survival rate for NSCLC patients remains largely unsatisfactory [3]. Accordingly, un-derstanding the molecular mechanisms that underlie the development of NSCLC is of critical importance to the identification of novel ther-apeutic strategies for this fatal disease.