Uc.63+ contributes to gastric cancer progression through regulation of NF-kB signaling
- 22 April 2020
- journal article
- research article
- Published by Springer Science and Business Media LLC in Gastric Cancer
- Vol. 23 (5), 863-873
- https://doi.org/10.1007/s10120-020-01070-8
Abstract
Background The transcribed ultraconserved regions (T-UCRs) are a novel class of long non-coding RNAs and are involved in the development of several types of cancer. Although several different papers have described the oncogenic role of Uc.63+, there are no reports mentioning its importance in gastric cancer (GC) biology. Methods In this study, we evaluated Uc.63+ expression using clinical samples of GC by qRT-PCR, and also assessed the correlation between Uc.63+ expression and clinico-pathological factors. Results The upregulation of Uc.63+ was significantly correlated with advanced clinico-pathological features. Knockdown of Uc.63+ significantly repressed GC cell growth and migration, whereas overexpression of Uc.63+ conversely promoted those of GC cells. In situ hybridization of Uc.63+ revealed its preferential expression in poorly differentiated adenocarcinoma. We further conducted a microarray analysis using MKN-1 cells overexpressing Uc.63- and found that NF-κB signaling was significantly upregulated in accordance with Uc.63+ expression. Conclusion Our results suggest that Uc.63+ could be involved in GC progression by regulating GC cell growth and migration via NF-κB signalingKeywords
Funding Information
- Japan Society for the Promotion of Science (JP15H04713)
- Japan Society for the Promotion of Science (JP16K08691, JP16H06999, 26670175, JP16K15247)
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