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神经元物质P通过细胞外RNA-TLR7轴驱动转移

Veena Padmanaban¹, Isabel Keller¹, Ethan S Seltzer¹

¹Laboratory of Systems Cancer Biology, The Rockefeller University, New York, NY, USA.

|August 7, 2024

概括

瘤内化导致乳腺癌转移. 针对神经物质P (SP) 途径,阿普雷皮坦抑制了瘤的生长和扩散,揭示了新的治疗策略.

科学领域:

癌症学
神经科学
免疫学

背景情况:

瘤内化与各种癌症患者的不良结果相关.
在高度转移的乳腺瘤中增加的神经存在表明在转移调节中的作用.

研究的目的:

研究瘤内置在乳腺癌转移中的作用.
阐明感觉神经元影响瘤进展的机制.
在神经癌症轴中确定潜在的治疗点.

主要方法:

在具有不同转移潜力的小鼠乳腺瘤中分析瘤内置.
研究SLIT2在瘤血管中的作用及其对内化的影响.
使用3D共同培养和体内模型研究P (SP) 对乳腺癌细胞的影响.
检查正在死亡的癌细胞,释放的ssRNA和Toll-like受体7 (TLR7) 之间的相互作用.
在临床前模型中评估TACR1抗剂的疗效.

主要成果:

高度转移的瘤表现出由SLIT2驱动的瘤血管内化增加.
乳腺癌细胞诱导感官神经元中的活动,导致物质P (SP) 的释放.
神经性SP促进了瘤生长,侵袭和转移,与患者的淋巴结扩散相关.
在高TACR1的癌细胞中,SP诱导的死亡释放了激活TLR7的ssRNA,从而促进了转移基因表达程序.
这种SP和ssRNA诱导的TLR7特征与乳腺癌存活率的降低有关.
在多个模型中,阿普雷皮坦治疗抑制了乳腺癌的生长和转移.

结论:

由感觉神经元衍生的SP驱动的瘤内化促进乳腺癌的生长和转移.
一个涉及神经信号,ssRNA释放和TLR7激活的新轴有助于转移性进展.
使用阿普雷皮坦向塔基宁受体1 (TACR1) 提供了潜在的乳腺癌治疗策略.

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