本研究旨在探讨microRNA调控ALDH1纤维肉瘤肿瘤细胞生物学行为的机制。我们鉴定了ALDH NMFH-1细胞中差异表达的miRNA，并在TCGA数据库中筛选与肉瘤转移相关的基因，最终获得参与转移的miRNA调控的关键基因。然后在细胞水平上验证这些关键基因的功能和机制。使用 ULCAN 数据库，发现 hsa-mir-206 与肉瘤患者的死亡率之间存在显着相关性。 WGCNA 分析鉴定出 352 个与肿瘤转移相关的基因。通过维恩图，我们获得了hsa-mir-206调控的15个转移相关基因。生存分析显示SYNPO2表达与生存率显着相关，并且在多种肿瘤中显着低表达。 SYNPO2与巨噬细胞呈负相关，与CD8 T细胞呈正相关。用siRNA质粒抑制hsa-mir-206的表达后，SYNPO2的mRNA表达显着上调。 CCK8实验、划痕实验、Transwell实验结果显示，抑制SYNPO2后NFMH-1细胞的增殖和迁移能力得到促进。 ALDH1肿瘤干细胞通过hsa-mir-206抑制SYNPO2促进恶性纤维组织细胞瘤细胞的增殖和侵袭。版权所有©2024。Elsevier Inc.出版。

This research aims to explore the mechanism by which microRNAs may regulate the biological behavior of tumor cells in ALDH1+ fibrosarcoma. We identified differentially expressed miRNAs in ALDH+ NMFH-1 cells, screened genes related to sarcoma metastasis in the TCGA database, and finally obtained key genes regulated by miRNAs that are involved in metastasis. The function and mechanism of these key genes were then validated at the cellular level. Using the ULCAN database, a significant correlation was found between hsa-mir-206 and mortality in sarcoma patients. WGCNA analysis identified 352 genes related to tumor metastasis. Through Venn diagrams, we obtained 15 metastasis-related genes regulated by hsa-mir-206. Survival analysis showed that SYNPO2 expression is significantly correlated with survival rate and is significantly underexpressed in multiple tumors. SYNPO2 showed a negative correlation with macrophages and a positive correlation with CD8+ T cells. After inhibiting the expression of hsa-mir-206 with siRNA plasmids, the mRNA expression of SYNPO2 was significantly upregulated. The results of CCK8 assay, scratch assay, and transwell assay showed that the proliferation and migration ability of NFMH-1 cells were promoted after SYNPO2 was inhibited. ALDH1+ tumor stem cells promote the proliferation and invasion of malignant fibrous histiocytoma cells by inhibiting SYNPO2 through hsa-mir-206.Copyright © 2024. Published by Elsevier Inc.