STAT4 介导的 miR-3619-5p 下调通过调节 TBC1D10B 促进胃腺癌。
STAT4-mediated down-regulation of miR-3619-5p facilitates stomach adenocarcinoma by modulating TBC1D10B.
机构信息
Department of Pathology, Wannan Medical College First Affiliated Hospital, Yijishan Hospital , Wuhu, Anhui Province, China.
Department of Cardiothoracic Surgery, Wannan Medical College First Affiliated Hospital, Yijishan Hospital , Wuhu, Anhui Province, China.
出版信息
Cancer Biol Ther. 2020 Jul 2;21(7):656-664. doi: 10.1080/15384047.2020.1754690. Epub 2020 May 13.
BACKGROUND
MicroRNAs (miRNAs) as the subtype of non-coding RNAs are revealed to be crucial players in cellular activities. It has been reported that miR-3619-5p functions as a tumor inhibitor in several cancers. However, the connection between miR-3619-5p and stomach adenocarcinoma (STAD) remains to be discovered.
AIM OF THE STUDY
The purpose of the study is to figure out the role and molecular regulation mechanism of miR-3619-5p in STAD.
METHODS
The expression of miR-3619-5p was evaluated via qRT-PCR analysis. Gain-of-function experiments demonstrated the effects of miR-3619-5p on cellular functions. The upper-stream transcription factor STAT4 and downstream target gene TBC1D10B of miR-3619-5p were identified by bioinformatic analysis. The binding and interaction between the indicated molecules were verified by RNA pull-down and luciferase reporter assays.
RESULTS
The expression of miR-3619-5p was prominently down-regulated in STAD cells and tissues. MiR-3619-5p suppresses cell proliferation, migration, invasion and tumor growth in STAD. Further, STAT4 bound with miR-3619-5p promoter and inhibited its transcription. MiR-3619-5p was also recognized to modulate STAD progression through the regulation of downstream target gene TBC1D10B.
CONCLUSION
STAT4-mediated miR-3619-5p controls STAD carcinogenesis and progression through modulating TBC1D10B expression, which may provide a novel insight for researching the STAD-related molecular mechanism.
背景
微小 RNA（miRNAs）作为非编码 RNA 的亚型，被揭示为细胞活动中的关键参与者。已有报道称，miR-3619-5p 在几种癌症中作为肿瘤抑制剂发挥作用。然而，miR-3619-5p 与胃腺癌（STAD）之间的联系仍有待发现。
研究目的
本研究旨在探讨 miR-3619-5p 在 STAD 中的作用和分子调控机制。
方法
通过 qRT-PCR 分析评估 miR-3619-5p 的表达。功能获得实验表明 miR-3619-5p 对细胞功能的影响。通过生物信息学分析确定 miR-3619-5p 的上游转录因子 STAT4 和下游靶基因 TBC1D10B。通过 RNA 下拉和荧光素酶报告基因实验验证指示分子之间的结合和相互作用。
结果
miR-3619-5p 在 STAD 细胞和组织中表达明显下调。miR-3619-5p 抑制 STAD 中的细胞增殖、迁移、侵袭和肿瘤生长。此外，STAT4 与 miR-3619-5p 启动子结合并抑制其转录。miR-3619-5p 还通过调节下游靶基因 TBC1D10B 来调节 STAD 进展。
结论
STAT4 介导的 miR-3619-5p 通过调节 TBC1D10B 表达控制 STAD 癌发生和进展，这可能为研究 STAD 相关分子机制提供新的见解。
Zotero 插件