期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 234, 期 7, 页码 11999-12010出版社
WILEY
DOI: 10.1002/jcp.27861
关键词
BTG1; DGCR5; gastric cancer; miR-23b; progression; PTEN
资金
- National Science Foundation of China [81500193, 81802409]
- Social Development Foundation of Zhenjiang [SH2018072, SH2018057]
- Natural Science Foundation of Jiangsu Province [BK20161353]
- Key Youth Talents Program in Health, Jiangsu Province [QNRC2016454]
Long noncoding RNA (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) has been reported to correlate with a variety of cancers, with its expression pattern and potential mechanism not clarified in gastric cancer (GC). In this study, we demonstrated that DGCR5 was downregulated in cancerous tissues and plasma samples frompatients with GC, and its downregulation was associated with advanced TNM stage and positive lymphatic metastasis. Plasma DGCR5 had an area under the receiver operating characteristic curve (AUC) of 0.722 for diagnosis of GC. Gain- and loss-of-function of DGCR5 revealed that DGCR5 functioned as a competing endogenous RNA for miR-23b to suppress GC cell proliferation, invasion and migration, and facilitate apoptosis by regulating PTEN and BTG1 in vitro. Furthermore, the overexpression of DGCR5 suppressed tumor growth, and inhibited the expression of miR-23b and proliferation antigen Ki-67, but increased the expression of PTEN and BTG1 in vivo. In conclusion, our results show that DGCR5 is a tumor-suppressive lncRNA that regulates PTEN and BTG1 expression through directly binding to miR-23b. This mechanism may contribute to a better understanding of GC pathogenesis and provide a potential therapeutic strategy for GC.
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