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.

中文翻译：

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STAT4 介导的 miR-3619-5p 下调通过调节 TBC1D10B 促进胃腺癌。

背景

MicroRNAs (miRNAs) 作为非编码 RNA 的亚型被揭示是细胞活动中的关键参与者。据报道，miR-3619-5p 在多种癌症中起到肿瘤抑制剂的作用。然而，miR-3619-5p与胃腺癌（STAD）之间的联系仍有待发现。

研究目的

本研究旨在阐明miR-3619-5p在STAD中的作用及分子调控机制。

方法

通过 qRT-PCR 分析评估 miR-3619-5p 的表达。功能获得实验证明了 miR-3619-5p 对细胞功能的影响。通过生物信息学分析鉴定了miR-3619-5p的上游转录因子STAT4和下游靶基因TBC1D10B。指定分子之间的结合和相互作用通过 RNA pull-down 和荧光素酶报告基因检测进行验证。

结果

miR-3619-5p 的表达在 STAD 细胞和组织中显着下调。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 也被认为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 表达来控制 STAD 的癌变和进展，这可能为研究 STAD 相关的分子机制提供新的见解。