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脂肪干细胞衍生的癌症相关纤维细胞抑制FGFR抑制剂的有效性

Mikhail G Kolonin¹, Dimitris Anastassiou²

¹The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center, Houston, Texas.

Cancer research

|March 4, 2024

概括

肥胖会促进癌症的进展. 脂肪细胞前体细胞分泌神经调节素1 (NRG1),在泌尿腺癌中引起对纤维细胞生长因子受体 (FGFR) 抑制剂的耐药性,这种耐药性可以用pertuzumab向.

科学领域:

在瘤学瘤学.
细胞生物学细胞生物学
分子医学是分子医学.

背景情况:

肥胖与增加癌症的攻击性和进展有关.
脂肪组织在促进瘤生长方面发挥着重要作用.
纤维细胞生长因子受体 (FGFR) 抑制剂是最近的治疗发展.

研究的目的:

确定脂肪细胞前体细胞对癌症进展有所贡献的机制.
为了研究尿路细胞癌如何对像erdafitinib这样的FGFR抑制剂产生抗性.
探索FGFR抑制剂耐药性的潜在治疗干预措施.

主要方法:

分析脂肪细胞前体细胞和尿癌细胞之间对膜信号的分析.
确定参与阻力的主要信号分子.
利用单细胞RNA测序数据来分析人类瘤中的细胞群.
测试pertuzumab在阻断已识别的抗药途径方面的疗效.

主要成果:

脂肪细胞前体细胞分泌神经调节素1 (NRG1),激活HER3信号传递,并赋予FGFR抑制剂的耐药性.
NRG1-介导的耐药性可以通过pertuzumab克服,这是一个针对NRG1/HER3轴的抗体.
人类瘤中的NRG1表达细胞类似于炎症性癌症相关纤维细胞 (iCAF),与脂肪 stromal 细胞 (ASC) 和纤维-基原生细胞 (FAP) 共享基因特征.

结论:

由脂肪细胞衍生细胞分泌的NRG1是尿路癌中FGFR抑制剂耐药性的新机制.
NRG1/HER3轴代表了克服抗性的潜在治疗目标.
确定的机制可能代表一种泛癌现象,有助于瘤的攻击性.

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