Long non-coding RNA DLEU1 predicts poor prognosis of gastric cancer and contributes to cell proliferation by epigenetically suppressing KLF2

Currently, accumulating documents have paid great attention to the critical role of long non-coding RNAs. The long non-coding RNAs DLEU1 has been demonstrated to be dysregulated in many solid tumors and hematological malignancies. However, the detailed descriptions about its potential roles and mole...

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Bibliographic Details
Published in:Cancer gene therapy 2018-04, Vol.25 (3-4), p.58-67
Main Authors: Li, Xiaobin, Li, Zongze, Liu, Ziwen, Xiao, Jianchun, Yu, Shuting, Song, Yimin
Format: Article
Language:English
Subjects:
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Apoptosis
Biomedicine
Cancer
Cancer metastasis
Cancer research
Cell cycle
Cell Proliferation
Epigenesis, Genetic
Female
Gastric cancer
Gene Expression
Gene Expression Regulation, Neoplastic
Gene Therapy
Genetic aspects
Humans
Krueppel-like factor
Kruppel-Like Transcription Factors - biosynthesis
Kruppel-Like Transcription Factors - genetics
Lymph nodes
Lysine
Male
Metastases
Neoplasm Proteins - biosynthesis
Neoplasm Proteins - genetics
Non-coding RNA
Prognosis
RNA
RNA, Long Noncoding - biosynthesis
RNA, Long Noncoding - genetics
RNA, Neoplasm - biosynthesis
RNA, Neoplasm - genetics
Solid tumors
Stomach cancer
Stomach Neoplasms - genetics
Stomach Neoplasms - metabolism
Transcription
Tumors
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Summary:Currently, accumulating documents have paid great attention to the critical role of long non-coding RNAs. The long non-coding RNAs DLEU1 has been demonstrated to be dysregulated in many solid tumors and hematological malignancies. However, the detailed descriptions about its potential roles and molecular mechanism in gastric cancer (GC) are still blurry. As for our research, it was found out that DLEU1 was observably intensified in GC tissues and cell lines. And highly expressed DLEU1 was relevant to tumor size, advanced stage of pathology and lymph node metastasis in GC patients. Silenced DLEU1 obviously suppressed proliferation via leading to the cell cycle arrest and inducing cell apoptosis of GC. Furthermore, mechanistic experiments uncovered that DLEU1 could recruit LSD1 (lysine specific demethylase 1) to the promoter regions of KLF2 and then suppressed its transcription. In addition, rescue assays revealed that the oncogenic function mediated by DLEU1 in GC was partly by regulating KLF2. Collectively, our findings manifested that DLEU1 might serve as an oncogene in GC.
ISSN:0929-1903
1476-5500
DOI:10.1038/s41417-017-0007-9