肝癌细胞衍生的外泌体SNORD52通过激活JAK2/STAT6信号通路介导M2巨噬细胞极化。
Hepatoma cell-derived exosomal SNORD52 mediates M2 macrophage polarization by activating the JAK2/STAT6 pathway.
作者信息
Zhang Yaqiong, Li Bo, Gu Wanhong, Fan Linna, Wang Xiaofan, Xu Meifen, Zhu Minqi, Jin Chong
机构信息
Department of Clinical Laboratory, Taizhou Central Hospital (Taizhou University Hospital), No.999 Donghai Road, Taizhou, 318000, Zhejiang, China.
Department of Ultrasound, Taizhou Hospital, Zhejiang University, Taizhou Enze Medical Center (Group), Taizhou, 318000, Zhejiang, China.
出版信息
Discov Oncol. 2025 Jan 13;16(1):36. doi: 10.1007/s12672-024-01700-y.
BACKGROUND
A recent study revealed the oncogenic role of box C/D small nucleolar RNA 52 (SNORD52) in hepatocellular carcinoma (HCC) by facilitating the aggressive phenotypes of hepatoma cells. However, the potential role of exosomal SNORD52 in macrophage polarization during HCC progression remains poorly understood.
METHODS
Exosomes were isolated from hepatoma cells. Western blotting and flow cytometry were performed to determine the levels of M2 macrophage polarization markers. SNORD52 expression was assessed using qRT-PCR. The levels of JAK2/STAT6 pathway-related proteins were analyzed using western blotting.
RESULTS
SNORD52 was enriched in exosomes derived from hepatoma cells and in plasma samples from patients with HCC. Hepatoma cell-derived exosomal SNORD52 was internalized by THP-1 macrophages. SNORD52 overexpression increased the levels of M2 macrophage polarization markers and JAK2/STAT6 pathway-related proteins Additionally, hepatoma cell-derived exosomal SNORD52 interacted with the JAK2/STAT6 pathway to mediate M2 macrophage polarization.
CONCLUSIONS
Our findings revealed that hepatoma cell-derived exosomal SNORD52 induces M2 macrophage polarization by activating the JAK2/STAT6 pathway.
背景
最近一项研究揭示了盒C/D小核仁RNA 52（SNORD52）通过促进肝癌细胞的侵袭性表型在肝细胞癌（HCC）中的致癌作用。然而，外泌体SNORD52在HCC进展过程中巨噬细胞极化中的潜在作用仍知之甚少。
方法
从肝癌细胞中分离外泌体。进行蛋白质免疫印迹和流式细胞术以确定M2巨噬细胞极化标志物的水平。使用qRT-PCR评估SNORD52的表达。使用蛋白质免疫印迹分析JAK2/STAT6通路相关蛋白的水平。
结果
SNORD52在肝癌细胞来源的外泌体和HCC患者的血浆样本中富集。肝癌细胞来源的外泌体SNORD52被THP-1巨噬细胞内化。SNORD52的过表达增加了M2巨噬细胞极化标志物和JAK2/STAT6通路相关蛋白的水平。此外，肝癌细胞来源的外泌体SNORD52与JAK2/STAT6通路相互作用以介导M2巨噬细胞极化。
结论
我们的研究结果表明，肝癌细胞来源的外泌体SNORD52通过激活JAK2/STAT6通路诱导M2巨噬细胞极化。
Zotero 插件