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- Title
Uc.63+ contributes to gastric cancer progression through regulation of NF-kB signaling.
- Authors
Sakamoto, Naoya; Sekino, Yohei; Fukada, Kaho; Pham, Quoc Thang; Honma, Ririno; Taniyama, Daiki; Ukai, Shoichi; Takashima, Tsuyoshi; Hattori, Takuya; Naka, Kazuhito; Tanabe, Kazuaki; Ohdan, Hideki; Yasui, Wataru
- 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 signaling
- Subjects
STOMACH cancer; NF-kappa B; CANCER invasiveness; CELL migration; IN situ hybridization
- Publication
Gastric Cancer, 2020, Vol 23, Issue 5, p863
- ISSN
1436-3291
- Publication type
Article
- DOI
10.1007/s10120-020-01070-8