Uc.63+contributes to gastric cancer progression through regulation of NF-kB signaling

被引：11

作者：

Sakamoto, Naoya ^{[1
]}

Sekino, Yohei ^{[1
]}

Fukada, Kaho ^{[1
]}

Quoc Thang Pham ^{[1
]}

Honma, Ririno ^{[1
]}

Taniyama, Daiki ^{[1
]}

Ukai, Shoichi ^{[1
]}

Takashima, Tsuyoshi ^{[1
]}

Hattori, Takuya ^{[1
]}

Naka, Kazuhito ^{[2
]}

Tanabe, Kazuaki ^{[3
]}

Ohdan, Hideki ^{[3
,4
]}

Yasui, Wataru ^{[1
]}

机构：

[1] Hiroshima Univ, Grad Sch Biomed & Hlth Sci, Dept Mol Pathol, Minami Ku, 1-2-3 Kasumi, Hiroshima 7348551, Japan

[2] Hiroshima Univ, Res Inst Radiat Biol & Med, Dept Stem Cell Biol, Hiroshima, Japan

[3] Hiroshima Univ, Grad Sch Biomed & Hlth Sci, Dept Hlth Care Adults, Hiroshima, Japan

[4] Hiroshima Univ, Grad Sch Biomed & Hlth Sci, Dept Gastroenterol & Transplant Surg, Hiroshima, Japan

来源：

GASTRIC CANCER | 2020年 / 23卷 / 05期

基金：

日本学术振兴会;

关键词：

Transcribed ultraconserved region; Gastric cancer; Uc; 63+; NF-kappa B; TRANSCRIBED ULTRACONSERVED REGION; NONCODING RNA; EXPRESSION; CARCINOMA; HYPERMETHYLATION; LIVER;

D O I：

10.1007/s10120-020-01070-8

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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-kappa B 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-kappa B signaling

引用

页码：863 / 873

页数：11

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