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赛马福林3C (Sema3C) 重塑树叶微环境,促进肝细胞癌的进展

Hao Peng¹, Meng Yang², Kun Feng³

¹Medical School, Southeast University, Nanjing, 210009, China.

Signal transduction and targeted therapy

|July 2, 2024

概括

肝细胞癌 (HCC) 的进展涉及癌症干细胞 (CSC) 和瘤微环境之间的交叉声. 在HCC上调节的Sema3C驱动这种相互作用,促进瘤生长和索拉芬尼布耐药性.

科学领域:

肝细胞癌 (HCC) 研究研究
瘤微环境 (TME) 动态
癌症干细胞 (CSC) 的生物学

背景情况:

超过90%的HCC病例发生在纤维化或肝硬化肝脏中,突出显示了TME的作用.
癌症相关纤维细胞 (CAF) 和CSC之间的相互作用对HCC进展至关重要.
通过CSCs影响HCC瘤层的机制尚不清楚.

研究的目的:

研究Sema3C在HCC发育和进展中的作用.
阐明HCC TME中涉及Sema3C的信号通路和分子相互作用.
评估Sema3C作为HCC的治疗点.

主要方法:

在肝脏组织,血液样本和HCC细胞 (包括抗索拉芬尼布的模型) 中分析Sema3C表达.
识别Sema3C受体 (NRP1,ITGB1) 和下游信号通道 (AKT/Gli1/c-Myc,NF-kB).
在体内研究评估Sema3C对细胞外基质,肝星细胞 (HSC) 和瘤生长的影响;阻断Sema3C.

主要成果:

塞马3C在纤维化肝脏,HCC组织,患者血液和抗索拉芬尼布的HCC中显著上调.
塞马3C的过度表达与茎状性相关,并通过NRP1/ITGB1.1促进HCC的自我更新和瘤启动.
塞马3C增强了HSC激活,原沉积和IL-6释放,与CAF衍生的TGF-β1.1形成了一个积极的反循环.
阻止Sema3C抑制瘤生长,并使HCC对索拉芬尼布敏感.

结论:

在HCC中,Sema3C是CSC和瘤层之间的交叉通话的关键媒介.
塞马3C作为肝癌发生的新型生物标志物.
向Sema3C提供了一个有希望的策略,以提高HCC治疗效率和克服耐药性.

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