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辐射重新编程纤维细胞,以驱动前列腺癌治疗耐药性

Anisha Madhav¹, Manish Thiruvalluvan¹, Frank Duong¹

¹Cedars-Sinai Cancer, Cedars-Sinai Medical Center, Los Angeles, California, USA.

Endocrine-related cancer

|November 25, 2025

概括

通过向BMP/CD105通路来克服前列腺癌 (PCa) 中的辐射抵抗. 阻断CD105信号与carotuximab通过破坏代谢支持,减少瘤生长,使PCa细胞对辐射敏感.

科学领域:

在瘤学瘤学.
癌症生物学癌症生物学
放射治疗研究放射治疗研究

背景情况:

放射治疗是局部性前列腺癌 (PCa) 的首要治疗方法.
抗辐射性显著阻碍PCa的治疗疗效.
瘤微环境在癌症进展和治疗反应中起着至关重要的作用.

研究的目的:

调查BMP/CD105信号通路在前列腺癌辐射抵抗中的作用.
阐明瘤微环境中辐射诱导的代谢转变.
评估用卡罗图克西马布向CD105的治疗潜力,以增强辐射敏感性.

主要方法:

利用前列腺瘤模型和纤维细胞培养.
进行了代谢分析,以确定关键的代谢酶和产品.
使用卡罗图西马布 (ENV105) 来阻止BMP/CD105信号传输.
在小鼠模型中评估瘤生长和DNA损伤 (皮下和 орто托普).

主要成果:

辐射诱导了BMP/CD105依赖的代谢转变,增加了β-基酸盐的产生.
这种代谢支持增强了PCa细胞的存活率和辐射后的DNA修复.
用carotuximab阻断CD105降低了β-基酸盐,增加了DNA损伤,并诱导了亡.
在临床前模型中,carotuximab和辐射的联合治疗显示出优异的瘤体积减少.

结论:

BMP/CD105轴是前列腺癌中辐射抵抗的关键调解器.
用carotuximab向纤维细胞CD105是一种有前途的策略,可以改善放射治疗的结果.
破坏瘤微环境中的代谢交叉会增强辐射的抗癌效应.

关键词:

纤维细胞细胞是什么?子子子子前列腺癌是前列腺癌.辐射电阻辐射电阻

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