EpCAM+微颗粒中miR-1266-5p调控Th17分化促进MPE的机制

Patients with malignant pleural effusion (MPE), the severe manifestation of primary or metastatic pleural tumors, is very difficult to control and patients with MPE got a poor prognosis. We previously found epithelial cell adhesion molecule-positive microparticles (ie EMPs) promoted MPE progression. Secondly, EMPs and miR-1266-5p enriched in EMPs were significantly higher in MPE than benign pleural effusion and miR-1266-5p in EMPs is significantly was negatively correlated with Th17 cells in MPE. Thirdly, miR-1266-5p in EMPs inhibited Th17 differentiation in vitro. Based on this, the project intends to do mechanism studies on how miR-1266-5p in EMPs regulate Th17 differentiation to develop MPE:①Elucidate the relationship among miR-1266-5p in EMPs, Th17 and the prognosis of patients in MPE.②Explore the mechanism of miR-1266-5p in EMPs regulates Th17 differentiation in vitro.③Verify the mechanism of miR-1266-5p in EMPs to facilitate MPE by regulating Th17 differentiation in mice bering Lewis models of MPE. Our research will provide a new perspective target MPE for clinical prevention and treatment lung cancer.

恶性胸腔积液（MPE）是原发或转移性胸膜肿瘤进展的严重表现,极难控制,患者预后差。我们前期研究发现：上皮细胞黏附分子阳性微颗粒（EpCAM+Microparticles即EMPs）促进MPE进展；在MPE中，EMPs及其富集的miR-1266-5p显著高于良性胸水，且EMPs中miR-1266-5p高表达与Th17负相关；体外EMPs中miR-1266-5p抑制Th17分化。. 基于此，拟就EMPs中miR-1266-5p调控Th17分化促进MPE的机制开展：①临床水平阐明EMPs中miR-1266-5p、Th17与预后的关系。②细胞水平探究EMPs中miR-1266-5p调控Th17分化的机制。③动物水平验证EMPs中miR-1266-5p调控Th17分化促MPE的机制，该研究将为靶向MPE防治肺癌提供新思路。

背景：恶性胸腔积液（MPE）是原发或转移性胸膜肿瘤进展的严重表现,极难控制,患者预后差。EMPs中miR-1266-5p调控Th17分化促进MPE的机制不明确。.研究内容为：①临床水平阐明EMPs中miR-1266-5p、Th17与预后的关系。②细胞水平探究EMPs中miR-1266-5p调控Th17分化的机制。③动物水平验证EMPs中miR-1266-5p调控Th17分化促MPE的机制。.研究结果：1.miR-1266-5p在多种腺癌(肺腺癌、胃腺癌)及多种肿瘤中高表达。我们证实miR-1266-5p 在肺腺癌（LUAC）组织及肺腺癌细胞来源的 MPs 中高表达.肿瘤细胞来源EMPs中miR-1266-5p与TNM及临床分期有关，与Th17细胞相关。2.生物信息学及细胞水平揭示 miR-1266-5p 下游靶基因参与 Th17 分化。.科学意义：为靶向microRNAs和TH17在肺腺癌治疗提供思路。