Li Jiajia, Li Zhongyu, Bai Xue, Chen Xiaofeng, Wang Meng, Wu Yanping, Wu Haotian
Department of Hematology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233000, China.
Bengbu Medical College, Bengbu, Anhui 233030, China.
J Oncol. 2022 Feb 8;2022:2756986. doi: 10.1155/2022/2756986. eCollection 2022.
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 . 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 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.
越来越多的研究证明，m6A甲基化在不同癌症中发挥着关键作用。然而，长链非编码RNA（lncRNA）如何调节m6A甲基化并参与急性髓系白血病（AML）仍不清楚。因此，本研究旨在通过调节m6A甲基化来探索UCA1在AML中的功能和机制。
采用qRT-PCR、蛋白质免疫印迹法和免疫组织化学染色检测METTL14、CXCR4和CYP1B1的表达。采用qRT-PCR检测UCA1的表达。分别采用CCK8、流式细胞术和Transwell实验检测HL60和U937细胞的增殖、凋亡、迁移和侵袭能力。采用斑点印迹分析检测m6A甲基化。建立荷瘤小鼠模型，并分析肿瘤重量和体积。采用免疫荧光染色、共定位和RNA下拉实验证实UCA1与METTL14之间的相互作用。
UCA1的过表达促进AML的发展。此外，我们发现受METTL14影响的m6A甲基化会受到UCA1的影响。UCA1通过调节m6A甲基化促进AML的发展。此外，CYP1B1和CXCR4的表达受METTL14的影响。此外，UCA1通过影响m6A甲基化促进AML的发展。
在本研究中，我们证明lncRNA UCA1通过影响METTL14的稳定性上调CXCR4和CYP1B1的表达，从而促进AML的进展。
