Suppr超能文献

急性髓系白血病细胞黏附于骨髓,并通过下调UNC5B的表达获得化学抗性。

Acute myeloid leukemia cells adhere to bone marrow and acquire chemoresistance by downregulating UNC5B expression.

作者信息

Teng Teng, Ren Liping, Xiao Jilong, Shi Zhiyu, Li Lanbo, Song Chunhong

机构信息

Shandong Key Laboratory of Traditional Chinese Medicine and Stress Injury, Department of Laboratory Animal Center, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.

Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.

出版信息

Front Oncol. 2024 Sep 24;14:1394443. doi: 10.3389/fonc.2024.1394443. eCollection 2024.

Abstract

Acute myeloid leukemia (AML) is a malignant tumor of the hematological system. Because of its characteristics of recurrence, refractory and chemoresistance, new therapeutic targets need to be identified. Adhesion and proliferation are characteristics of AML cells, and critical steps in inducing chemotherapy resistance. In this study, we reported that UNC5B inhibits AML cell bone marrow adhesion, inhibits AML cell proliferation and increases sensitivity to chemotherapy. Mechanistically, RNA sequencing (RNA-seq) and experimental results revealed that overexpression of UNC5B inhibits adhesion and proliferation signaling pathways and inhibits the expression of MPZL1, CLDN23, IGF2 and WNT7B. In conclusion, our findings suggest that UNC5B serves as a prognostic indicator and a potential therapeutic target for AML.

摘要

急性髓系白血病(AML)是一种血液系统恶性肿瘤。由于其具有复发、难治和化疗耐药的特点,需要确定新的治疗靶点。黏附和增殖是AML细胞的特征,也是诱导化疗耐药的关键步骤。在本研究中,我们报道UNC5B可抑制AML细胞与骨髓的黏附,抑制AML细胞增殖并增加对化疗的敏感性。机制上,RNA测序(RNA-seq)和实验结果显示,UNC5B的过表达抑制黏附和增殖信号通路,并抑制MPZL1、CLDN23、IGF2和WNT7B的表达。总之,我们的研究结果表明UNC5B可作为AML的预后指标和潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a50/11460579/50b61d71046d/fonc-14-1394443-g001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验