CD81 通过阻断 CD274/PD-L1 的选择性自噬降解驱动放射抵抗性胶质母细胞瘤的免疫逃逸
CD81 drives immune evasion in radioresistant glioblastoma by blocking selective autophagic degradation of CD274/PD-L1.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Human umbilical cord mesenchymal stem cell-derived exosomes carrying hsa-miRNA-128-3p suppress pancreatic ductal cell carcinoma by inhibiting Galectin-3.
Human umbilical cord mesenchymal stem cell-derived exosomes carrying hsa-miRNA-128-3p suppress pancreatic ductal cell carcinoma by inhibiting Galectin-3.
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Hsa-miRNA-128-3p 可被视为胰腺癌的潜在治疗方法。我们为 PDAC 的靶向治疗提供了一种新思路。
胰腺导管腺癌(PDAC)是消化系统最致命的恶性肿瘤之一。许多患者确诊时已处于晚期,失去手术机会。此外,治疗胰腺导管细胞癌的有效方法很少。microRNA(miRNA)及其在肿瘤进展中的调控作用日益受到关注。在本研究中,我们探讨了携带hsa-miRNA-128-3p的人脐带间充质干细胞(HUCMSCs)来源外泌体对胰腺癌细胞的影响。
基于现有实验和数据库信息,我们选择了与胰腺癌相关的Galectin-3及其对应的上游hsa-miRNA-128-3p。我们从新鲜脐带中提取HUCMSCs,将hsa-miRNA-128-3p转染至HUCMSCs中,并提取和收集含有hsa-miRNA-128-3p的外泌体。分析了富含hsa-miRNA-128-3p的外泌体对胰腺癌细胞的影响。
Galectin-3在正常胰腺导管上皮细胞中的表达显著低于PDAC细胞系。我们成功从脐带中提取了HUCMSCs,并将hsa-miRNA-128-3p转染至HUCMSCs中。随后我们证明,携带hsa-miRNA-128-3p的HUCMSC来源外泌体可通过靶向Galectin-3在体外抑制PANC-1细胞的增殖、侵袭和迁移。
Pancreatic ductal adenocarcinoma (PDAC) is one of the most fatal malignant tumors of the digestive system. Many patients are diagnosed at an advanced stage and lose eligibility for surgery. Moreover, there are few effective methods for treating pancreatic ductal cell carcinoma. Increasing attention has been given to microRNAs (miRNAs) and their regulatory roles in tumor progression. In this study, we investigated the effects of exosomes extracted from human umbilical cord mesenchymal stem cells (HUCMSCs) carrying hsa-miRNA-128-3p on pancreatic cancer cells.
Based on existing experimental and database information, we selected Galectin-3, which is associated with pancreatic cancer, and the corresponding upstream hsa-miRNA-128-3p. We extracted HUCMSCs from a fresh umbilical cord, hsa-miRNA-128-3p was transfected into HUCMSCs, and exosomes containing hsa-miRNA-128-3p were extracted and collected. The effect of exosomes rich in hsa-miRNA-128-3p on pancreatic cancer cells was analyzed.
The expression of Galectin-3 in normal pancreatic duct epithelial cells was significantly lower than that in PDAC cell lines. We successfully extracted HUCMSCs from the umbilical cord and transfected hsa-miRNA-128-3p into HUCMSCs. Then we demonstrated that HUCMSC-derived exosomes with hsa-miRNA-128-3p could suppress the proliferation, invasion, and migration of PANC-1 cells in vitro by targeting Galectin-3.
Hsa-miRNA-128-3p could be considered as a potential therapy for pancreatic cancer. We provided a new idea for targeted therapy of PDAC.
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