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外体SLC16A1-AS1诱导的M2巨细胞两极化促进肝细胞癌的进展

Yuhang Hu¹, Yang Li¹, Hewei Xiong¹

¹Department of Emergency Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

International journal of biological sciences

|September 9, 2024

概括

肝细胞癌 (HCC) 外体含有SLC16A1-AS1,它通过将巨细胞偏向到M2来驱动瘤生长. 这促进了HCC的进展,并建议SLC16A1-AS1作为潜在的治疗点.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

巨细胞是瘤微环境 (TME) 中的关键免疫细胞,通过细胞-细胞通信影响瘤的发展.
外基因组调解细胞间通信,但它们在协调瘤细胞和免疫细胞通过肝细胞癌 (HCC) 中 lncRNAs 相互作用中的作用尚不清楚.

研究的目的:

研究外体长非编码RNAs (lncRNAs) 在肝细胞癌 (HCC) 细胞间通信中的作用.
阐明外体SLC16A1-AS1调节巨细胞极化并促进HCC进展的机制.

主要方法:

从HCC细胞中获得的外体lncRNAs的分析.
研究SLC16A1-AS1与巨细胞中的HNRNPA1和SLC16A1mRNA的相互作用.
评估巨细胞M2极化及其对HCC细胞增殖,入侵和糖解的影响.
对涉及IL-6,STAT3,METTL3和SLC16A1-AS1.1的相互信号循环的评估.

主要成果:

由HCC外基因组衍生的SLC16A1-AS1通过诱导M2巨细胞极化促进HCC恶性进展.
通过HNRNPA1相互作用,SLC16A1-AS1增强了巨细胞中的SLC16A1mRNA稳定性,增加了乳酸运输和激活c-Raf/ERK信号.
在M2巨细胞分泌IL-6的地方存在一个相互循环,激活HCC细胞中的STAT3和METTL3,这反过来稳定了SLC16A1-AS1.1.

结论:

外体SLC16A1-AS1作为一个信号分子,诱导乳酸介导的M2巨细胞两极分化在HCC.
在HCC细胞和M2巨细胞之间识别的SLC16A1-AS1/IL-6信号轴促进瘤增殖,入侵和糖解.
SLC16A1-AS1代表了HCC治疗的潜在治疗标.

关键词:

在M2中,极化为M2.在SLC16A1-AS1中,我们有SLC16A1-AS1.外基因组是外基因组的组成部分.m6A 一个很好的.巨细胞是什么?巨细胞是什么?

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