ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2020
Uc.63+ contributes to gastric cancer progression through regulation of NF-kB signaling.
Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Enhanced ITGA3 expression induced by helicobacter pylori infection facilitates gastric cancer progression via NF-κB and Smad4.Molecular and cellular biochemistry · 2026Article
- The transcribed ultraconserved regions: emerging players in colorectal cancer biology and therapy.Frontiers in cell and developmental biology · 2025Review
- Exosome regulation of immune response mechanism: Pros and cons in immunotherapy.Bioactive materials · 2024Article
- Ultra-conserved RNA: a novel biological tool with diagnostic and therapeutic potential.Discover oncology · 2023Review
- Transcribed Ultraconserved Regions: New regulators in cancer signaling and potential biomarkers.Genetics and molecular biology · 2023Article
- Long noncoding RNA uc.230/CUG-binding protein 1 axis sustains intestinal epithelial homeostasis and response to tissue injury.JCI insight · 2022Article
- Role of transcribed ultraconserved regions in gastric cancer and therapeutic perspectives.World journal of gastroenterology · 2022Review
- New insights into exosome mediated tumor-immune escape: Clinical perspectives and therapeutic strategies.Biochimica et biophysica acta. Reviews on cancer · 2021Review
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe 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.
methodsIn 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.
resultsThe 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.
conclusionOur 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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.