circ_0006089 通过调节 miR-361-3p/TGFB1 促进胃癌生长、转移、糖酵解和血管生成,Cancer Science

当前位置： X-MOL 学术 › Cancer Sci. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

circ_0006089 通过调节 miR-361-3p/TGFB1 促进胃癌生长、转移、糖酵解和血管生成
Cancer Science ( IF 4.5 ) Pub Date : 2022-03-29 , DOI: 10.1111/cas.15351
Ying Zhou ₁ , Qilin Zhang ₂ , Bingling Liao ₁ , Xiaofeng Qiu ₂ , Sheng Hu ₂ , Qihua Xu ₁

Affiliation

环状 RNA (circRNA) 参与多种病理生理过程，包括胃癌 (GC) 的发展。然而，circ_0006089 在 GC 进展中的作用及其潜在的分子机制需要进一步揭示。定量实时 PCR 用于检测 circ_0006089、microRNA (miR)-361-3p 和转化生长因子-β1 (TGFB1) 的表达。使用双荧光素酶报告基因分析和 RNA 免疫沉淀 (RIP) 分析证实了 miR-361-3p 和 circ_0006089 或 TGFB1 之间的相互作用。使用集落形成测定、EdU测定、transwell测定、流式细胞术和管形成测定测定细胞增殖、转移、凋亡和血管生成。通过检测葡萄糖消耗、乳酸产生和 ATP 水平来评估细胞糖酵解。此外，蛋白质印迹（WB）分析用于测量蛋白质表达。异种移植肿瘤模型用于评估 circ_0006089 敲低对 GC 肿瘤发生的影响。已发现 circ_0006089 在 GC 组织和细胞中上调，它可以充当 miR-361-3p 海绵。circ_0006089 敲低抑制了 GC 增殖、转移、糖酵解、血管生成和增加细胞凋亡，而这种作用可以被 miR-361-3p 抑制剂撤销。TGFB1 被 miR-361-3p 靶向，其过表达逆转了 miR-361-3p 对 GC 细胞功能的影响。此外，circ_0006089 通过海绵化 miR-361-3p 促进 TGFB1 的表达。动物实验表明，沉默的 circ_0006089 通过 miR-361-3p/TGFB1 通路抑制 GC 肿瘤发生。我们的结果表明，circ_0006089/miR-361-3p/TGFB1 轴有助于 GC 进展，

"点击查看英文标题和摘要"

circ_0006089 promotes gastric cancer growth, metastasis, glycolysis, and angiogenesis by regulating miR-361-3p/TGFB1

Circular RNA (circRNA) participates in a variety of pathophysiological processes, including the development of gastric cancer (GC). However, the role of circ_0006089 in GC progression and its underlying molecular mechanism need to be further revealed. Quantitative real-time PCR was utilized for detecting circ_0006089, microRNA (miR)-361-3p and transforming growth factor-β1 (TGFB1) expression. The interaction between miR-361-3p and circ_0006089 or TGFB1 was confirmed using a dual-luciferase reporter assay and an RNA immunoprecipitation (RIP) assay. Cell proliferation, metastasis, apoptosis, and angiogenesis were determined using colony formation assay, EdU assay, transwell assay, flow cytometry, and tube formation assay. Cell glycolysis was evaluated by detecting glucose consumption, lactate production, and ATP levels. In addition, western blot (WB) analysis was used to measure protein expression. Xenograft tumor models were used to assess the effect of circ_0006089 knockdown on GC tumorigenesis. circ_0006089 had been found to be upregulated in GC tissues and cells, and it could act as an miR-361-3p sponge. circ_0006089 knockdown suppressed GC proliferation, metastasis, glycolysis, angiogenesis, and increased apoptosis, while this effect could be revoked by miR-361-3p inhibitor. TGFB1 was targeted by miR-361-3p, and its overexpression reversed the effects of miR-361-3p on GC cell function. Also, circ_0006089 promoted TGFB1 expression via sponging miR-361-3p. Animal experiments showed that silenced circ_0006089 inhibited GC tumorigenesis through the miR-361-3p/TGFB1 pathway. Our results revealed that the circ_0006089/miR-361-3p/TGFB1 axis contributed to GC progression, confirming that circ_0006089 might be a potential therapeutic target for GC.

更新日期：2022-03-29

点击分享查看原文

点击收藏

公开下载

阅读更多本刊新发论文本刊介绍/投稿指南