在脂肪细胞-瘤微环境中的代谢和信号相互作用
1Natural Products & Nanobiotechnology Research Lab, Department of Community Medicine, Saveetha Medical College and Hospital, Saveetha Institute of Medical and Technical Sciences (SIMATS), (Saveetha University), Thandalam, Chennai, Tamil Nadu 602 105, India.
The Journal of steroid biochemistry and molecular biology
|November 18, 2025
概括
脂肪细胞通过促进瘤生长和治疗耐药性来促进三阴性乳腺癌 (TNBC) 和口腔状细胞癌 (OSCC) 等攻击性癌症. 针对这种代谢交叉的目标提供了新的治疗策略.
科学领域:
- 在瘤学瘤学.
- 癌症生物学 癌症生物学
- 代谢信号传递 代谢信号传递
背景情况:
- 脂肪细胞是癌症进展和治疗耐药性的活性调节者.
- 它们通过代谢,免疫和信号通路与瘤细胞相互作用.
- 这种交叉声会促进瘤细胞的增殖,干性和生存.
研究的目的:
- 在三阴性乳腺癌 (TNBC) 和口腔状细胞癌 (OSCC) 中审查脂肪细胞-瘤交叉.
- 检查脂细胞衍生媒介如何影响瘤的攻击性和治疗结果.
- 突出脂肪细胞分泌的因素及其瘤原体信号作用.
主要方法:
- 关于脂肪细胞与瘤相互作用的科学文献的综述.
- 对脂肪细胞分泌的因素的分析 (例如,补充C3,CXCL12,勒丁,阿迪波内克丁).
- 检查由脂肪细胞和其他介质调节的分子通路 (例如CXCL12/CXCR4-PI3K/AKT,HIF-1α,NF-κB,β-catenin,mTOR).
主要成果:
- 像C3和CXCL12这样的脂肪细胞衍生因素促进了TNBC和OSCC的瘤生长,干性和治疗抵抗.
- 特定的途径,如C3/C3aR激活,可以增强OSCC的茎状性.
- 在TNBC中由双甲诱导的CXCL12激活CXCL12/CXCR4-PI3K/AKT轴,驱动上皮细胞-介质细胞过渡和抵抗.
- 循环RNA和代谢酶 (例如GCLC) 调节关键的致癌途径.
结论:
- 脂肪细胞建立了一个支持瘤的利基,大大促进了治疗耐药性.
- 向脂肪细胞与瘤相互作用可以抑制瘤原体信号传递并恢复治疗灵敏度.
- 破坏代谢交叉声提供了针对TNBC和OSCC等侵袭性癌症的新组合策略.
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