Research Papers:
Regulation of laryngeal squamous cell cancer progression by the lncRNA H19/miR-148a-3p/DNMT1 axis
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Abstract
Tianyi Wu1,*, Lingmei Qu2,*, Guoqing He1,*, Linli Tian1,*, Liang Li1, Han Zhou1, Qian Jin1, Jingyuan Ren3, Yu Wang1, Jingting Wang1, Xuan Kan1, Ming Liu1, Jia Shen4, Mian Guo5, Yanan Sun1
1Department of Otorhinolaryngology, Head and Neck Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China
2Department of Otorhinolaryngology, Head and Neck Surgery, The Fifth Affiliated Hospital of Harbin Medical University, Daqing, China
3Department of Head and Neck Surgery, The Oncology Hospital of Jilin province, Changchun, China
4Department of Orthopaedic Surgery and the Orthopaedic Hospital Research Center, University of California, Los Angeles, California, USA
5Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China
*These authors contributed equally to this work
Correspondence to:
Yanan Sun, e-mail: [email protected]
Mian Guo, e-mail: [email protected]
Keywords: laryngeal squamous cell cancer, lncRNA H19, miR-148a-3p, DNMT1
Received: July 07, 2015 Accepted: December 05, 2015 Published: February 08, 2016
ABSTRACT
Laryngeal squamous cell carcinoma (LSCC) is a highly aggressive malignant cancer. The regulation of LSCC progression by long non-coding RNA (lncRNA) was not well understood. In this study, we reported that the lncRNA H19 was upregulated in LSCC. The expression levels of H19 were inversely correlated with the survival rate of LSCC patients. Knockdown of H19 expression inhibited LSCC cell migration, invasion and proliferation. We identified microRNA miR-148a-3p as an inhibitory target for H19. Overexpression of miR-148a-3p reduced LSCC migration, invasion and proliferation cell, while inhibition of miR-148a-3p did the opposite. The inhibition of LSCC progression induced by H19 knockdown required the activity of miR-148a-3p. We also identified DNA methyltransferase enzyme DNMT1 as a target of miR-148a-3p. Cellular DNA methylation levels were inhibited by both miR-148a-3p overexpression and H19 knockdown. In summary, our study demonstrated that the lncRNA H19 promoted LSCC progression via miR-148a-3p and DNMT1.
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