H-B Ge1, S Chen, S-R Huang, J Zhu. 1. Department of Respiratory Medicine, Third Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China. jsnjzj@163.com.
Abstract
OBJECTIVE: Recent researches have proved the important role of long noncoding RNAs (lncRNAs) in many diseases. In this study, the potential function of lncRNA ZFAS1 in the development of non-small cell lung cancer (NSCLC) was mainly explored. PATIENTS AND METHODS: ZFAS1 expression in NSCLC patients was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay, colony formation assay and ethynyl deoxyuridine (EdU) incorporation assay were conducted to evaluate the regulatory effects of ZFAS1 on cellular behaviors of the NSCLC cells. Furthermore, the interaction between ZFAS1 and miR-193a-3p in mediating the progression of NSCLC was elucidated. RESULTS: ZFAS1 expression was significantly higher in NSCLC samples relative to adjacent tissues. The proliferation of NSCLC cells was inhibited by silence of ZFAS1, and conversely, ZFAS2 overexpression promoted the proliferative ability. Further experiments showed that miR-193a-3p was directly targeted by ZFAS1. CONCLUSIONS: ZFAS1 could enhance cell growth ability of NSCLC by targeting miR-193a-3p, suggesting that ZFAS1 may be a potential therapeutic target in NSCLC.
OBJECTIVE: Recent researches have proved the important role of long noncoding RNAs (lncRNAs) in many diseases. In this study, the potential function of lncRNA ZFAS1 in the development of non-small cell lung cancer (NSCLC) was mainly explored. PATIENTS AND METHODS: ZFAS1 expression in NSCLCpatients was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay, colony formation assay and ethynyl deoxyuridine (EdU) incorporation assay were conducted to evaluate the regulatory effects of ZFAS1 on cellular behaviors of the NSCLC cells. Furthermore, the interaction between ZFAS1 and miR-193a-3p in mediating the progression of NSCLC was elucidated. RESULTS:ZFAS1 expression was significantly higher in NSCLC samples relative to adjacent tissues. The proliferation of NSCLC cells was inhibited by silence of ZFAS1, and conversely, ZFAS2 overexpression promoted the proliferative ability. Further experiments showed that miR-193a-3p was directly targeted by ZFAS1. CONCLUSIONS:ZFAS1 could enhance cell growth ability of NSCLC by targeting miR-193a-3p, suggesting that ZFAS1 may be a potential therapeutic target in NSCLC.