Research Papers:
Long intergenic noncoding RNA 00673 promotes non-small-cell lung cancer metastasis by binding with EZH2 and causing epigenetic silencing of HOXA5
PDF | HTML | Supplementary Files | How to cite
Metrics: PDF 2835 views | HTML 2872 views | ?
Abstract
Chenhui Ma1,2,3,*, Guannan Wu1,2,*, Qingqing Zhu1,2, Hongbing Liu1,2, Yanwen Yao1,2, Dongmei Yuan1,2, Yafang Liu1,2,4, Tangfeng Lv1,2, Yong Song1,2
1Department of Respiratory Medicine, Jinling Hospital, Nanjing 210002, China
2Nanjing University Institute of Respiratory Medicine, Nanjing 210002, China
3Nanjing Medical University Affiliated Wuxi Second Hospital, Wuxi 214002, China
4Nanfang Hospital, Southern Medical University, Guangzhou 510515, China
*These authors contributed equally to this work
Correspondence to:
Tangfeng Lv, email: [email protected]
Yong Song, email: [email protected]
Keywords: long noncoding RNA, linc00673, NSCLC, metastasis, HOXA5
Received: January 02, 2017 Accepted: February 15, 2017 Published: March 13, 2017
ABSTRACT
Metastasis of cancer cells is a key impediment to favorable outcomes of cancer treatment. Functional roles of long noncoding RNAs in several biological processes, including metastasis, have recently been discovered. In our previous work, we reported a positive correlation of increased expression of linc00673 in NSCLC tissues with tumor size, lymph node metastasis, TNM stage, and increased proliferation of NSCLC cells, both, in vitro and in vivo. In this study, we demonstrate that ectopic expression of linc00673 promotes migration and invasion of NSCLC cells. Furthermore, our results indicate that linc00673 could silence HOXA5 expression by recruiting epigenetic repressor, EZH2, at its promoter regions. HOXA5 was identified as a tumor suppressor gene, which inhibited NSCLC cell metastasis by regulating cytoskeletal remodeling. To summarize, we for the first time identified the role of lin00673 in promoting invasion and migration of NSCLC cells. Insights from this study may help to identify novel therapeutic targets for NSCLC.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 16158