Matrine exerted an anti-tumor effect on acute myeloid leukemia via the lncRNA LINC01116/miR-592-mediated JAK/STAT pathway inactivation

苦参碱通过 lncRNA LINC01116/miR-592 介导的 JAK/STAT 通路失活对急性髓系白血病发挥抗肿瘤作用

阅读:9
作者:Ping-Ping Zhang, Feng Zhang, Kai Zhu, Jun-Feng Zhu, Yuan Yuan, Yan-Li Yang, Lin Liu, Meng Wang, Jia-Jia Li

Abstract

As a malignant hematological cancer, acute myeloid leukemia (AML) influences the health of many people. This study explored the anti-AML activity of matrine (a natural-derived alkaloid), as well as the internal molecular mechanism. In vitro, cell viability, apoptosis, and productions of inflammatory cytokines including IL-1β, IL-6, and TNF-α were tested by MTT, Annexin V-FITC/PI staining, and ELISA, respectively. The expression levels of LINC01116 and miR-592 were measured by qRT-PCR. Bcl-2 and PCNA expression, and JAK/STAT3 pathway activity were evaluated by western blotting. Besides, an AML mouse xenograft model was established to further analyze the anti-AML activity of matrine. We found that matrine suppressed cell proliferation and levels of inflammatory factors, induced cell apoptosis, reduced LINC01116 expression, and raised miR-592 expression in AML cells. LINC01116 directly bound to miR-592 and downregulated its expression. Both LINC01116 overexpression and miR-592 knockdown attenuated the effects of matrine on AML cells. Moreover, miR-592 overexpression reversed the influences of LINC01116 overexpression on matrine-treated AML cells. Matrine inactivated the JAK/STAT3 pathway in AML cells via modulating LINC01116/miR-592. Additionally, matrine inhibited tumor growth via modulating LINC01116/miR-592 in vivo. To sum up, matrine exhibited the anti-AML activity through regulating the LINC01116/miR-592 axis, thereby inactivating the JAK/STAT3 pathway.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。