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GL-V9通过丝裂原活化蛋白激酶(MAPK)信号通路诱导慢性粒细胞白血病(CML)细胞凋亡。

GL-V9 induce apoptosis of CML cells via MAPK signaling pathway.

作者信息

Jiang Fengyu, Xue Yangyang, Zhang Qin, Ma Tonghui, Li Yongming, Yu Xiaoxuan

机构信息

Jiangsu Collaborative Innovation Center of Chinese Medicinal Resources Industrialization, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, PR China.

State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, 210023, PR China.

出版信息

Heliyon. 2024 Jul 3;10(14):e34030. doi: 10.1016/j.heliyon.2024.e34030. eCollection 2024 Jul 30.

Abstract

GL-V9, a derivative of wogonin, has shown potent antitumor effects in various cancers, yet its impact on chronic myeloid leukemia (CML) remains unexplored. In this study, we found that GL-V9 significantly decreased the viability of CML cells. Annexin V/PI staining demonstrated that GL-V9 induced apoptosis in a concentration-dependent manner. The JC-1 assay indicated a significant reduction in mitochondrial membrane potential (ΔΨm) in cells treated with GL-V9. Additionally, GL-V9 altered reactive oxygen species (ROS) levels in CML cells. Through transcriptomic sequencing and Western blot analysis, we further revealed that GL-V9 activated the MAPK pathway. These results suggest that GL-V9 is a promising therapeutic candidate for CML.

摘要

汉黄芩素衍生物GL-V9在多种癌症中已显示出强大的抗肿瘤作用,但其对慢性粒细胞白血病(CML)的影响仍未得到探索。在本研究中,我们发现GL-V9显著降低了CML细胞的活力。Annexin V/PI染色表明GL-V9以浓度依赖的方式诱导细胞凋亡。JC-1检测表明,用GL-V9处理的细胞中线粒体膜电位(ΔΨm)显著降低。此外,GL-V9改变了CML细胞中的活性氧(ROS)水平。通过转录组测序和蛋白质印迹分析,我们进一步揭示GL-V9激活了MAPK通路。这些结果表明,GL-V9是一种有前景的CML治疗候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ab8/11295560/0938b578a156/gr1.jpg

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