Long non-coding RNA LUCAT1 is associated with poor prognosis in human non-small cell lung cancer and regulates cell proliferation via epigenetically repressing p21 and p57 expression
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Yue Sun1,*, Shi-Dai Jin2,*, Quan Zhu3,*, Liang Han4,6,*, Jing Feng1,5, Xi-Yi Lu2, Wei Wang3, Feng Wang3, Ren-Hua Guo2
1Department of Oncology, Yancheng Third People’s Hospital, The Affiliated Yanchen Hospital of Southeast University Medicine College, Yancheng, Jiangsu, China
2Department of Oncology, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
3Department of Thoracic Surgery, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
4Department of Oncology, Xuzhou Central Hospital, Affiliated Xuzhou Hospital, College of Medicine, Southeast University, Xuzhou, Jiangsu, China
5Department of Oncology, Jiangsu Shengze Hospital, Suzhou, Jiangsu, China
6Department of Oncology, Yancheng Third People’s Hospital, The Affiliated Yanchen Hospital of Southeast University Medicine College, Yancheng, Jiangsu, China
*These authors contributed equally to this work and should be regarded as joint first authors
Ren-Hua Guo, email: firstname.lastname@example.org
Keywords: LncRNAs, LUCAT1, p21, p57, non-small cell lung cancer (NSCLC)
Received: June 09, 2016 Accepted: February 27, 2017 Published: March 09, 2017
Recently, long non-coding RNAs (lncRNAs) have been recognized as playing key roles in regulating cellular processes, such as proliferation, invasion, and metastasis. These lncRNAs have been shown to be abnormally expressed in tumorigenic processes. However, the role and clinical relevance of LUCAT1 in non-small-cell lung cancer (NSCLC) remain unclear. In this study, we found that the expression of LUCAT1 was significantly up-regulated in NSCLC tissues compared to non-tumor tissues, and its expression was associated with tumor size, tumor–node–metastasis (TNM) stage and overall survival (OS). Further experiments showed that LUCAT1 knockdown inhibited cell proliferation both in vitro and in vivo. Mechanistic investigations showed that LUCAT1 plays a key role in G0/G1 arrest. We further demonstrated that LUCAT1 was associated with polycomb repressor complexes (PRC2) and that this association was required for epigenetically repression of p21 and p57, thus contributing to the regulation of NSCLC cell cycle and proliferation. In summary, our results show that LUCAT1 could regulate tumorigenesis of NSCLC and be biomarker for poor prognosis in NSCLC.
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