瘤细胞对脂肪细胞的SAA1依赖性重编程与三重阴性乳腺癌的攻击性有关
Ilona Rybinska1, Nunzia Mangano1, Sandra L Romero-Cordoba2,3
1Microenvironment and Biomarkers of Solid Tumors Unit, Department of Experimental Oncology, Fondazione IRCCS Istituto Nazionale dei Tumori di Milano, Milan, Italy.
International journal of cancer
|January 30, 2024
概括
三重阴性乳腺癌 (TNBC) 的进展涉及瘤细胞和脂肪细胞的相互作用. 这项研究确定了血清粉样蛋白A1 (SAA1) 作为一个关键的媒介,将脂肪细胞重编程与TNBC攻击性联系起来.
科学领域:
- 在瘤学瘤学.
- 癌症生物学 癌症生物学
- 免疫学 免疫学 免疫学
背景情况:
- 由于有限的向疗法,三阴性乳腺癌 (TNBC) 的预后不佳.
- 瘤进展受到瘤内在因素,瘤微环境和宿主特征的影响.
- 脂肪细胞,关键的乳腺层细胞,在癌症中表现出可塑性,但瘤-脂肪细胞交叉的瘤衍生媒介在很大程度上是未知的.
研究的目的:
- 为了识别TNBC细胞和脂肪细胞之间的交叉语音的分子媒介.
- 阐明这种交叉语音在TNBC进展和攻击性中的作用.
- 研究瘤-脂肪细胞相互作用对瘤微环境的影响.
主要方法:
- 在体外共同培养TNBC细胞和脂肪细胞的模型.
- 转录概况分析用于分析细胞反应.
- 免疫细胞招募和细胞因子生产 (CXCL5,IL-8) 的分析.
- 对血清粉样蛋白A1 (SAA1) 信号通路的研究 (CD36,P2XR7).
- 在人类TNBC组织中检查SAA1表达.
主要成果:
- TNBC-脂肪细胞交叉诱导与炎症和瘤微环境相互作用相关的独特转录特征.
- 交叉声增强了癌症干状特征,并通过CXCL5和IL-8招募了亲瘤原生免疫细胞.
- SAA1被确定为通过CD36和P2XR7信号的脂肪细胞重编程的调节者.
- 在人类TNBC中,SAA1表达与脂肪细胞透,炎症,脂解,茎状性质和独特的免疫微环境相关.
结论:
- 由SAA1调解的TNBC-脂肪细胞相互作用显著促进TNBC的攻击性.
- 脂肪细胞的SAA1重编程影响TNBC进展的关键方面,包括干细胞和免疫细胞透.
- 针对SAA1介导的交叉声可能为TNBC提供新的治疗策略.
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