Expression of Concern
This article is currently under investigation. We strongly recommend that this article is not cited until the investigation is completed.
Research Paper Volume 11, Issue 14 pp 4990—5007

Long noncoding RNA FALEC inhibits proliferation and metastasis of tongue squamous cell carcinoma by epigenetically silencing ECM1 through EZH2

Bo Jia1,2, *, , Tao Xie3, *, , Xiaoling Qiu1, , Xiang Sun1, , Jun Chen1, , Zhijie Huang1, , Xianghuai Zheng1, , Zhiping Wang1, , Jianjiang Zhao1, ,

  • 1 Department of Oral Surgery, Stomatological Hospital, Southern Medical University, Guangzhou 510280, People’s Republic of China
  • 2 Department of Stomatology, Shunde Hospital, Southern Medical University, Foshan 528300, People’s Republic of China
  • 3 Department of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou 510280, People’s Republic of China
* Equal contribution.

Received: April 17, 2019       Accepted: July 10, 2019       Published: July 23, 2019
How to Cite

Copyright © 2019 Jia et al. This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Tongue squamous cell carcinoma (TSCC), the most common epithelial cancer identified in the oral cavity, has become one of the most common malignancies across the developing countries. Increasing evidence indicates that long non-coding RNAs (lncRNAs) serve as important regulators in cancer biology. The focally amplified long non-coding RNA in epithelial cancer (FALEC) was found downregulated in the tissues of tongue squamous cell carcinoma (TSCC) and was predicted to present a good prognosis by bioinformatics analysis. Experiments indicated that FALEC knockdown significantly increased the proliferation and migration of TSCC cells both in vitro and in vivo; however, FALEC overexpression repressed these malignant behaviors. RNA pull-down and RNA immunoprecipitation demonstrated that FALEC could recruit enhancer of zeste homolog 2 (EZH2) at the promoter regions of extracellular matrix protein 1 (ECM1), epigenetically repressing ECM1 expression. The data revealed that FALEC acted as a tumor suppressor in TSCC and may aid in developing a novel potential therapeutic strategy against TSCC.


lncRNAs: long noncoding RNAs; FALEC: focally amplified long non-coding RNA in epithelial cancer; TSCC: tongue squamous cell carcinoma; RT-qPCR: Reverse transcription-quantitative polymerase chain reaction; RIP: RNA immunoprecipitation; EZH2: enhancer of zeste homolog 2; ChIP: Chromatin immunoprecipitation; H3K27me3: histone H3 lysine 27 trimethylation; ECM1: Extracellular matrix protein 1; TCGA: the cancer Genome Atlas; GEO: Gene Expression Omnibus; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; ATCC: American Type Culture Collection; IHC: immunohistochemistry; PRC2: Polycomb repressive complex 2; EMT: epithelial–mesenchymal transition; ITGB4: integrin β4.