脂肪细胞衍生的IL6和三阴性乳腺癌细胞衍生的CXCL1共同激活STAT3/NF-κB通路,以调解脂肪细胞和三阴性乳腺癌细胞之间的交叉通话
在PubMed上查看摘要
概括
此摘要是机器生成的。肥胖会加重三阴性乳腺癌 (TNBC) 的结果. 脂肪细胞通过CXCL1和IL6信号促进TNBC入侵,激活STAT3/NF-κB通路,这表明TNBC的新治疗点.
科学领域
- 癌症学
- 细胞生物学
- 代谢综合征
背景情况
- 三重阴性乳腺癌 (TNBC) 的预后不佳,尤其是在与肥胖相关的情况下.
- 脂肪细胞与TNBC细胞的相互作用显著影响TNBC的进展.
研究的目的
- 阐明脂肪细胞和TNBC细胞之间的交叉交谈机制.
- 研究这种相互作用如何促进TNBC的进展.
主要方法
- 成熟脂肪细胞 (hADSC,3T3-L1) 和TNBC细胞的共同培养模型.
- 在体外测定 (伤口愈合,Transwell,RT-PCR,西部抹杀,ELISA) 和体内小鼠模型 (肥胖和瘤异种移植).
主要成果
- 共同培养增强了TNBC细胞的入侵.
- 脂肪细胞增加了CXCL1和IL6的分泌,通过STAT3/NF-κB激活在TNBC细胞中的MMP7/MMP9上调.
- 在体内模型证实了这些发现.
结论
- 在CXCL1和IL6的介导下,TNBC细胞与脂肪细胞之间存在显著的交叉对话.
- 这种相互作用激活了STAT3/NF-κB通路,促进了TNBC的进展.
- 已确定的途径为个性化TNBC治疗提供了潜在的目标.
相关概念视频
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