Journal
CANCER LETTERS
Volume 417, Issue -, Pages 47-57Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2017.12.016
Keywords
LUCAT1; DNA methyltransferase 1; Esophagus squamous cell carcinoma; Long-noncoding RNA; DNA methylation; Epigenetics
Categories
Funding
- Basic Science Research Program through the National Research Foundation of Korea - Korea government (Ministry of Science and ICT) [NRF-2017R1A2B4006316]
- Brain Korea 21 PLUS Project for Medical Science, Yonsei University
- Korea Health Technology R&D Project through the Korea Health Industry Development Institute
- Ministry of Health and Welfare [HI15C1578]
Ask authors/readers for more resources
Available targeted therapies for esophageal squamous cell carcinoma (ESCC) are limited; thus, further genetic and epigenetic studies are needed. Recently, many long noncoding RNAs (IncRNAs) 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. (C) 2017 Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available