Hsa_circ_0010882通过调节M1/M2巨细胞极化来促进肝细胞癌的进展
1Department of Medical Oncology, The Affiliated Xuzhou Municipal Hospital of Xuzhou Medical University, Xuzhou, China.
Journal of viral hepatitis
|January 18, 2024
概括
肝细胞癌 (HCC) 的进展与增加的circ_0010882有关,这促进了免疫抑制的M2巨细胞. 向circ_0010882可能通过改变巨细胞平衡来提供新的HCC治疗策略.
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:
- 肝细胞癌 (HCC) 是一种普遍存在的恶性瘤,其特点是免疫抑制性瘤微环境和患者的不良结果.
- 巨细胞两极分化,特别是M1/M2平衡,在调节瘤微环境和影响HCC进展方面发挥着至关重要的作用.
研究的目的:
- 这项研究旨在调查hsa_circ_0010882在M1/M2巨分化中在肝细胞癌进展的背景下发挥的作用.
- 这项研究旨在阐明circ_0010882影响巨细胞表型并影响HCC细胞行为的分子机制.
主要方法:
- 从接受肝切除术的患者中采集了配对的HCC组织样本 (n=125).
- 使用THP-1细胞诱导M1和M2巨细胞表型.
- 细胞实验评估了HCC细胞活力,迁移和与巨细胞和转染的HCC细胞共同培养后的入侵. 生物信息分析和双露西法酶记者测定被用来确认circ_0010882和miR-382.2之间的相互作用.
主要成果:
- 在HCC组织中,Circ_0010882的表达显著升高,与较短的整体存活率相关.
- 干扰circ_0010882促进了M1巨标记物 (TNF-α,iNOS),同时抑制了M2标记物 (Arg-1,CD206),表明从M2极化转移.
- 沉默circ_0010882增强了M1巨细胞介导的抑制HCC细胞活力,迁移和入侵,同时减少了M2巨细胞驱动的瘤促进. 确定了米R-382作为circ_0010882.2.的直接目标.
结论:
- 在HCC中,circ_0010882的表达上调,并与预后不佳有关.
- 沉默circ_0010882抑制HCC进展中的M2巨细胞极化,部分通过调节miR-382表达.
- Circ_0010882具有作为诊断生物标志物和治疗点的潜力,可以改善HCC治疗策略和患者的治疗结果.
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