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윤정호(내과학교실) Cancer Lett
등록일 : 2017-12-22 오후 8:34:00       조회 : 553
첨   부 :
제1저자 윤정호(내과학교실, BK21)
교신저자 이상길(내과학교실)

Cancer Lett. 2017 Dec 13. pii: S0304-3835(17)30788-7. doi: 10.1016/j.canlet.2017.12.016. [Epub ahead of print]
The long noncoding RNA LUCAT1 promotes tumorigenesis by controlling ubiquitination and stability of DNA methyltransferase 1 in esophageal squamous cell carcinoma.
Yoon JH1, You BH2, Park CH3, Kim YJ3, Nam JW4, Lee SK5.

Author information
1Brain Korea 21 PLUS Project for Medical Science, Yonsei University, Republic of Korea.2Department of Life Science, College of Natural Sciences, Hanyang University, Seoul 133791, Republic of Korea.3Division of Gastroenterology, Institute of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, Severance Hospital, Seoul, Republic of Korea.4Department of Life Science, College of Natural Sciences, Hanyang University, Seoul 133791, Republic of Korea; Research Institute for Convergence of Basic Sciences, Hanyang University, Seoul 133791, Republic of Korea.5Brain Korea 21 PLUS Project for Medical Science, Yonsei University, Republic of Korea; Division of Gastroenterology, Institute of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, Severance Hospital, Seoul, Republic of Korea. Electronic address: sklee@yuhs.ac.

Abstract
Available targeted therapies for esophageal squamous cell carcinoma (ESCC) are limited; thus, further genetic and epigenetic studies are needed. Recently, many long noncoding RNAs (lncRNAs) have been reported to be involved in various cancers. Here, we investigated whether the lncRNA LUCAT1 was related to the carcinogenesis of ESCC based on previous studies in lung cancer. LUCAT1 was significantly upregulated in ESCC cell lines and cancer tissue compared with normal cells and adjacent normal tissues. LUCAT1 knockdown reduced cell proliferation, induced apoptosis, and upregulated tumor-suppressor genes by reducing DNA methylation in KYSE-30 ;cells. Moreover, LUCAT1 siRNA reduced DNA methyltransferase 1 (DNMT1) protein levels without affecting transcription. Patients with high LUCAT1 expression had significantly lower survival rates than patients with low LUCAT1 expression. Our results thus suggest that LUCAT1 regulates the stability of DNMT1 and inhibits the expression of tumor suppressors through DNA methylation, leading to the formation and metastasis of ESCC. We identified LUCAT1 as a potential target for drug development and as a biomarker for ESCC.
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