Hsa_circ_0000092通过SMC1A对IL24进行上调,以诱导巨细胞M2极化
Rihai Ma1, Anmin Wang2, Meng Yang2
1Department of Hepatobiliary Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, Guangxi Zhuang Autonomous Region, 533000, China.
Heliyon
|September 19, 2024
概括
肝细胞癌 (HCC) 的进展与上皮细胞-介质细胞过渡 (EMT) 有关. 这项研究表明,circ_0000092通过上调IL24来促进HCC细胞EMT,从而诱导瘤相关巨细胞 (TAM) 的M2极化.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 肝细胞癌 (HCC) 是癌症死亡的主要原因.
- 在HCC中,上皮-介质细胞过渡 (EMT) 与转移和复发相关.
- 与瘤相关的巨细胞 (TAMs),特别是M2极化的巨细胞,可以在瘤微环境中增强HCC细胞EMT.
研究的目的:
- 阐明连接HCC细胞和TAMs的潜在分子机制.
- 调查has_circ_0000092在HCC进展和巨细胞极化中的作用.
主要方法:
- 使用定量实时PCR (RT-qPCR) 和西式斑点测试来评估RNA和蛋白质的表达.
- 进行了机制实验,以确定has_circ_0000092,U2AF2,SMC1A和IL24之间的关系.
- 进行了救援试验,以评估circ_0000092对TAM M2极化的影响.
主要成果:
- 在HCC细胞中检测到has_circ_0000092的高表达.
- 发现has_circ_0000092可以招募U2AF2,促进SMC1A的转录.
- 证明Circ_0000092通过增强HCC细胞中的IL24表达来调节TAMs的M2极化.
结论:
- Hsa_circ_0000092通过SMC1A.上调调节IL24的表达.
- 这一过程诱导了巨细胞的M2极化,导致HCC的进展.
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