165P - Long noncoding RNA LUCAT1 is associated with poor prognosis in human non-small cell lung cancer and affects cell proliferation via regulating p21 a...

Date 15 April 2016
Event European Lung Cancer Conference 2016 (ELCC) 2016
Session Poster lunch
Topics Translational Research
Non-Small Cell Lung Cancer
Basic Principles in the Management and Treatment (of cancer)
Presenter guo Renhua
Citation Journal of Thoracic Oncology (2016) 11 (supplement 4): S57-S166. S1556-0864(16)X0004-4
Authors G. Renhua, S. Yue, J. Shidai, F. Jing, L. Xiyi
  • Oncology, Jiangsu Provincial People’s Hospital (The First Affiliated Hospital of Nanjing Medical University), 210000 - Nanjing/CN



Recently, long non-coding RNAs (lncRNAs) is identified to play a key role in regulating cellular process, such as proliferation, invasion and metastasis. These lncRNAs are shown to be ectopic expressed in tumorigenic processes. However, the role and clinical relevance of LUCAT1 in non-small cell lung cancer (NSCLC) remain unclear.


Polymerase chain reaction (qPCR) assays was used to analyse the expression of LUCAT1 in non-small cell lung cancer (NSCLC) tissues and cell lines. MTT and colony formation assays were performed to evaluate the effect of LUCAT1 on proliferation, and flow cytometry was performed to evaluate cell apoptosis. The NSCLC cell lines were transfected with si-LUCAT1 and injected into nude mice to investigate the effect of LUCAT1 on oncogenesis in vivo. The connection between LUCAT1 and EZH2 was verified by RIP. The related protein levels of LUCAT1 targets were studied by ChIP.


The expression of LUCAT1 was obviously up-regulated in NSCLC cancer tissues compared to non-tumor tissues, and its expression was bound up with tumor size, tumor TNM stage, lymphatic metastasis and overall survival. Univariate and multivariate analyses revealed that LUCAT1 expression acted as an independent predictor for overall survival. Animal experiments significantly showed that the proliferation was inhibited by LUCAT1 knockdown both in vitro and in vivo. Furthermore, we also displayed that LUCAT1 played a crucial role in G1 arrest. What's more, we further affirmed that LUCAT1 was correlated with enhancer of zeste homolog 2 (EZH2) by repressing the expression of p21 and p57. Here, we first report the role and molecular mechanism of LUCAT1 in the NSCLC cellular processes.


Our results show that LUCAT1 could be a poor prognostic biomarker in NSCLC and regulate cancer biology.

Clinical trial identification

Legal entity responsible for the study

Jiangsu Provincial People's Hospital, Nanjing Medical University


The National Natural Science Foundation of China, The National Scientific Foundation of Jiangsu Provincial of China


All authors have declared no conflicts of interest.