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MMP11和MMP14有助于割抵抗性前列腺癌和脂肪细胞之间的相互作用

Bing Tan^1,2,3, Xiaoyu Zheng⁴, Xiaoqin Xie⁵

¹Department of Urology, University-Town Hospital of Chongqing Medical University Shapingba District, Chongqing 401331, China.

American journal of cancer research

|January 8, 2024

概括

矩阵金属蛋白酶 (MMPs),特别是MMP11和MMP14,通过影响脂肪细胞相互作用和脂质代谢,促进前列腺癌 (PCa) 的进展. 针对这些MMP显著抑制了割耐性前列腺癌 (CRPC) 的生长.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生物化学

背景情况:

脂肪细胞增强前列腺癌 (PCa) 的进展,有助于割抵抗性前列腺癌 (CRPC) 的发展.
连接脂肪细胞和CRPC进展的精确机制仍然不完全理解.
矩阵金属蛋白酶 (MMP) 是关键酶,参与细胞外矩阵重塑和因子激活.

研究的目的:

研究MMP11和MMP14在脂肪细胞和CRPC细胞之间的相互作用中的作用.
阐明MMPs促进CRPC进展的分子机制.
评估在CRPC治疗中准MMP11和MMP14的治疗潜力.

主要方法:

评估了PCa患者的MMP11表达,并将其与预后相关联.
在CRPC细胞和与脂肪细胞共同培养模型中利用siRNA敲除MMP11和MMP14.
分析了脂肪细胞脱脂的变化,CRPC脂质代谢,线粒体的形成和蛋白质的表达 (帕金,mTOR,HIF1α,MMP2,Ki67).
在MMP11/14敲击后,在异种移植小鼠模型中评估了瘤生长抑制.

主要成果:

在PCa患者中,MMP11表达升高,与预后不佳相关.
在CRPC细胞中MMP11的淘汰导致脂肪细胞脱脂和CRPC脂质吸收受损.
通过mTOR/HIF1α/MMP2通路减少CRPC细胞入侵和脂质代谢.
同时的MMP11/14淘汰在体内显著延迟瘤生长,降低脂质代谢和增加帕金水平.

结论:

MMP11和MMP14在脂肪细胞和CRPC细胞之间的交叉通话中发挥着关键作用.
准MMP11和MMP14有效地抑制CRPC进展和脂质代谢.
抑制MMP11/14是一种有前途的治疗策略,用于治疗CRPC患者.

关键词:

割抵抗性前列腺癌是什么?脂肪细胞的脂肪细胞.脂质新陈代谢脂质新陈代谢矩阵金属蛋白质酶的结构.线粒细胞衰变 (mitophagy) 是一种神经衰变的过程.

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