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雄激素受体通过调节 miR23a-3p/EPHB2 通路促进肺癌转移。

Androgen Receptor Promotes Lung Cancer Metastasis by Modifying the miR23a-3p/EPHB2 Pathway.

机构信息

Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

出版信息

Curr Med Sci. 2024 Oct;44(5):954-963. doi: 10.1007/s11596-024-2891-1. Epub 2024 Oct 11.

DOI:10.1007/s11596-024-2891-1
PMID:39390216
Abstract

OBJECTIVE

This study aimed to investigate the reasons behind the lower survival rates in male lung cancer patients than in female lung cancer patients.

METHODS

Through various techniques, such as Argonaute immunoprecipitation, luciferase assays, and ChIP, this study confirmed the positive effects of androgen receptor (AR) on lung cancer cell invasion across different in vitro cell lines and in vivo mouse models.

RESULTS

The findings suggest that AR enhanced the invasion of lung cancer cells by modifying EPHB2 signals at the protein expression level, which in turn required changes in miRNA-23a-3p. Restoring miRNA-23a-3p could counteract the intensified invasion of lung cancer cells mediated by AR.

CONCLUSION

This study revealed that AR may facilitate the lung cancer matastasis by modulating miRNA-23a-3p/EPHB2 signaling and that targeting this signaling pathway could provide new approaches to inhibit lung cancer metastasis.

摘要

目的

本研究旨在探讨男性肺癌患者生存率低于女性肺癌患者的原因。

方法

通过 Argonaute 免疫沉淀、荧光素酶测定和 ChIP 等多种技术,本研究证实了雄激素受体 (AR) 对不同体外细胞系和体内小鼠模型中肺癌细胞侵袭的积极影响。

结果

研究结果表明,AR 通过在蛋白质表达水平上修饰 EPHB2 信号来增强肺癌细胞的侵袭,这反过来又需要 miRNA-23a-3p 的变化。恢复 miRNA-23a-3p 可以抵消 AR 介导的肺癌细胞侵袭的增强。

结论

本研究揭示了 AR 可能通过调节 miRNA-23a-3p/EPHB2 信号促进肺癌转移,靶向该信号通路可能为抑制肺癌转移提供新的方法。

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