Uc. 63+ contributes to gastric cancer progression through regulation of NF-kB signaling
N Sakamoto, Y Sekino, K Fukada, QT Pham, R Honma… - Gastric Cancer, 2020 - Springer
N Sakamoto, Y Sekino, K Fukada, QT Pham, R Honma, D Taniyama, S Ukai, T Takashima…
Gastric Cancer, 2020•SpringerBackground 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 …
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 …
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
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