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mTORC1关闭释放了TFEB,可以驱动三阴性乳腺癌的入侵

Michalis Gounis¹, Hellyeh Hamidi¹, Johanna Ivaska²

¹Turku Bioscience Centre, University of Turku and Åbo Akademi University, 20520 Turku, Finland.

Developmental cell

|April 8, 2025

概括

在三阴性乳腺癌 (TNBC) 中抑制PI3K/AKT/mTOR通路可能不是理想的. 抑制mTORC1激活TFEB,增加细胞入侵和细胞外基质降解,特别是在化疗中.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

PI3K/AKT/mTOR通路是三阴性乳腺癌 (TNBC) 的一个公认的治疗标.
针对这种途径的目标是抑制癌细胞的增殖和生存.

研究的目的:

研究mTORC1抑制对TNBC进展的影响.
探索TFEB激活在对mTORC1抑制的反应中的作用.

主要方法:

利用分子生物学技术在TNBC模型中研究PI3K/AKT/mTOR途径.
评估了mTORC1抑制对TFEB活性,MT1-MMP表细胞分裂和细胞外基质 (ECM) 降解的影响.
评估了mTORC1抑制和化疗对细胞入侵的联合作用.

主要成果:

发现mTORC1抑制可以激活转录因子TFEB.
激活的TFEB促进了MT1-MMP的表细胞分解,这是一种参与ECM降解的酶.
增加ECM降解导致增强细胞入侵,特别是与化疗相结合时.

结论:

矛盾的是,mTORC1抑制可以通过激活TFEB来促进TNBC细胞入侵.
这些发现挑战了目前针对TNBCPI3K/AKT/mTOR途径的治疗策略.
需要进一步的研究来了解这种途径在TNBC治疗中的复杂作用.

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