甲基化
基因敲除
流式细胞术
RNA甲基化
免疫印迹
癌症研究
免疫组织化学
髓系白血病
小干扰RNA
细胞凋亡
生物
分子生物学
核糖核酸
免疫学
基因
生物化学
甲基转移酶
作者
Jiajia Li,Zhongyu Li,Xue Bai,Xiaofeng Chen,Meng Wang,Yanping Wu,Haotian Wu
摘要
Increasing numbers of studies have proved that m6A methylation plays crucial roles in different cancers. However, how lncRNA regulates m6A methylation and participates in acute myeloid leukemia (AML) remains unclear. Therefore, this study aims to explore the function and mechanism of UCA1 in AML by regulating m6A methylation.qRT-PCR, western blot, and immunohistochemical staining were used to detect the expression of METTL14, CXCR4, and CYP1B1. qRT-PCR was used to detect the expression of UCA1. CCK8, flow cytometry, and transwell assays were used to detect the proliferation, apoptosis, migration, and invasion of HL60 and U937 cells, respectively. m6A methylation was detected by dot blot analysis. Tumor-bearing mice were established, and tumor weight and volume were analyzed. Immunofluorescence staining, co-localization, and RNA pull-down were used to confirm the reaction between UCA1 and METTL14.Overexpression of UCA1 promotes AML development in vitro. Furthermore, we found that METTL14-influenced m6A methylation could be affected by UCA1. UCA1 promoted AML development by regulating m6A methylation. Moreover, the expression of CYP1B1 and CXCR4 was affected by METTL14. In addition, UCA1 promoted AML development by affecting m6A methylation in vivo.In the present study, we demonstrated that lncRNAUCA1 promotes the progression of AML by upregulating the expression of CXCR4 and CYP1B1 by affecting the stability of METTL14.
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