miR-495-3p下调ZWINT通过阻断p38 MAPK信号通路激活抑制乳腺癌肺转移。

IF 3.1 3区 生物学 Q3 CELL BIOLOGY
Ming-Tao Shao, Wei-Wen Li, Yong Li, Ping Chen, Shuai-Shuai Yu, Wen-Jie Lu, Chun-Mei Chen, Yan Dong, Yi-Wen Zhang, Qun-Chen Zhang
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引用次数: 0

摘要

乳腺癌转移是患者死亡的主要原因,但有效的治疗靶点仍然有限。基于我们之前确定的ZWINT作为与转移相关的预后标志物,本研究确定了它的关键功能作用和调节机制。多组学分析显示,ZWINT表达与乳腺癌亚型的转移过程有很强的相关性。在功能上,ZWINT敲低显著抑制乳腺癌细胞在体外的迁移和侵袭,显著减少体内的肺转移。在机制上,我们发现miR-495-3p直接靶向并抑制ZWINT表达,并且该miR-495-3p/ZWINT轴通过抑制p38 MAPK通路激活来抑制体外转移进展。我们的研究结果表明,ZWINT驱动乳腺癌转移,并受到miR-495-3p的负调控。新发现的miR-495-3p/ZWINT/p38 MAPK轴可能为抑制乳腺癌进展提供一个有希望的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
ZWINT down-regulated by miR-495-3p inhibited lung metastasis of breast cancer by blocking p38 MAPK signaling pathway activation.

Breast cancer metastasis is the primary cause of patient mortality, yet effective therapeutic targets remain limited. Building on our prior identification of ZWINT as a prognostic marker linked to metastasis, this study defines its critical functional role and regulatory mechanism. Multi-omics analysis revealed a strong association between ZWINT expression and metastatic processes across breast cancer subtypes. Functionally, ZWINT knockdown significantly inhibited breast cancer cell migration and invasion in vitro and dramatically reduced lung metastasis in vivo. Mechanistically, we discovered that miR-495-3p directly targets and suppresses ZWINT expression, and this miR-495-3p/ZWINT axis acts through inhibiting p38 MAPK pathway activation to suppress metastatic progression in vitro. Our findings demonstrate that ZWINT drives breast cancer metastasis and is negatively regulated by miR-495-3p. The newly identified miR-495-3p/ZWINT/p38 MAPK axis may provide a promising therapeutic target for suppressing breast cancer progression.

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来源期刊
Human Cell
Human Cell CELL BIOLOGY-
CiteScore
5.90
自引率
2.30%
发文量
176
审稿时长
4.5 months
期刊介绍: Human Cell is the official English-language journal of the Japan Human Cell Society. The journal serves as a forum for international research on all aspects of the human cell, encompassing not only cell biology but also pathology, cytology, and oncology, including clinical oncology. Embryonic stem cells derived from animals, regenerative medicine using animal cells, and experimental animal models with implications for human diseases are covered as well. Submissions in any of the following categories will be considered: Research Articles, Cell Lines, Rapid Communications, Reviews, and Letters to the Editor. A brief clinical case report focusing on cellular responses to pathological insults in human studies may also be submitted as a Letter to the Editor in a concise and short format. Not only basic scientists but also gynecologists, oncologists, and other clinical scientists are welcome to submit work expressing new ideas or research using human cells.
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