S-J Sun1, Q Lin, J-X Ma, W-W Shi, B Yang, F Li. 1. Department of Oncology, Chinese PLA General Hospital, Haidian, Beijing, China. lf30100@126.com.
Abstract
OBJECTIVE: The present study aimed to explore the role of long non-coding RNA NEAT1 (NEAT1) in mediating non-small cell lung cancer (NSCLC) cell migration and invasion, as well as the underlying regulatory mechanisms. PATIENTS AND METHODS: The NEAT1 expression in NSCLC tissues and cell lines was measured using reverse transcription‑quantitative polymerase chain reaction (RT-qPCR). The relationships between NEAT1 expression and clinicopathological parameters were examined by chi-square test. Overall survival curves were analyzed using the Kaplan-Meier method. Effects of NEAT1 on cell growth, invasion and migration were evaluated by cell counting kit-8 assay and transwell assay, respectively. Western blotting was used to address the impact of NEAT1 on Wnt/β‑catenin signaling. RESULTS: We observed that the expression of NEAT1 in NSCLC tissues and cell lines were much higher than that in normal control, respectively. High NEAT1 expression was statistically associated with poor differentiation, Lymph node metastasis and advanced TMN stage (all p < 0.05). According to the Kaplan-Meier survival analysis, NSCLC patients with high NEAT1expression had a significantly shorter overall survival than those with high NEAT1 expression(p < 0.001). Moreover, the downregulation of NEAT1 expression significantly inhibited the NSCLC cells proliferation, migration, and invasiveness. Finally, we found that decreased expression of NEAT1 inhibited the Wnt/β-catenin signaling pathway activity. CONCLUSIONS: Our data for the first time showed that NEAT1 contribute to the tumorigenesis and development of NSCLC by activating Wnt/β-catenin signaling pathway, suggesting that NEAT1 may provide a therapeutic strategy for the treatment of NSCLC patients.
OBJECTIVE: The present study aimed to explore the role of long non-coding RNA NEAT1 (NEAT1) in mediating non-small cell lung cancer (NSCLC) cell migration and invasion, as well as the underlying regulatory mechanisms. PATIENTS AND METHODS: The NEAT1 expression in NSCLC tissues and cell lines was measured using reverse transcription‑quantitative polymerase chain reaction (RT-qPCR). The relationships between NEAT1 expression and clinicopathological parameters were examined by chi-square test. Overall survival curves were analyzed using the Kaplan-Meier method. Effects of NEAT1 on cell growth, invasion and migration were evaluated by cell counting kit-8 assay and transwell assay, respectively. Western blotting was used to address the impact of NEAT1 on Wnt/β‑catenin signaling. RESULTS: We observed that the expression of NEAT1 in NSCLC tissues and cell lines were much higher than that in normal control, respectively. High NEAT1 expression was statistically associated with poor differentiation, Lymph node metastasis and advanced TMN stage (all p < 0.05). According to the Kaplan-Meier survival analysis, NSCLCpatients with high NEAT1expression had a significantly shorter overall survival than those with high NEAT1 expression(p < 0.001). Moreover, the downregulation of NEAT1 expression significantly inhibited the NSCLC cells proliferation, migration, and invasiveness. Finally, we found that decreased expression of NEAT1 inhibited the Wnt/β-catenin signaling pathway activity. CONCLUSIONS: Our data for the first time showed that NEAT1 contribute to the tumorigenesis and development of NSCLC by activating Wnt/β-catenin signaling pathway, suggesting that NEAT1 may provide a therapeutic strategy for the treatment of NSCLCpatients.
Authors: Mei S Ong; Wanpei Cai; Yi Yuan; Hin C Leong; Tuan Z Tan; Asad Mohammad; Ming L You; Frank Arfuso; Boon C Goh; Sudha Warrier; Gautam Sethi; Nicholas S Tolwinski; Peter E Lobie; Celestial T Yap; Shing C Hooi; Ruby Y Huang; Alan P Kumar Journal: Br J Pharmacol Date: 2017-08-23 Impact factor: 8.739