GIPC2 is a tumor suppressor gene for acute myeloid leukemia and induces apoptosis of leukemia cells by regulating the PI3K/AKT pathway

被引：0
|
作者：
Zhao, Jingyuan [1 ,3 ]
Liu, Jinnan [3 ]
Liu, Sichu [3 ]
Tian, Siyu [2 ]
Yuan, Hong [2 ,3 ]
Li, Shuai [4 ]
机构：
[1] Dalian Med Univ, Affiliated Hosp 1, Stem Cell Clin Res Ctr, Dalian, Peoples R China
[2] Dalian Municipal Cent Hosp, Clin Lab Ctr, Dalian, Peoples R China
[3] Dalian Med Univ, Coll Lab Sci, Dalian, Peoples R China
[4] Dalian Med Univ, Affiliated Hosp 1, Dept Pharm, Dalian, Peoples R China
来源：
EPIGENOMICS | 2023年 / 15卷 / 06期
基金：
中国国家自然科学基金;
关键词：
AML; apoptosis; GIPC2; methylation; PI3K; AKT; CANCER; PROLIFERATION; MUTATIONS;
D O I：
10.2217/epi-2023-0027
中图分类号：
Q3 [遗传学];
学科分类号：
071007 ; 090102 ;
摘要：
Aims: To explore the expression and methylation levels of GIPC2 in acute myeloid leukemia (AML), discuss the mechanism of GIPC2 in AML and provide new strategies for the diagnosis and treatment of AML. Methods: qPCR, western blotting, cell counting kit-8 assay, bisulfite sequencing and other experiments were used in this study. Results: The expression of GIPC2 was found to be downregulated in AML and is mainly affected by DNA promoter methylation. Decitabine can demethylate the promoter region of GIPC2, and GIPC2 expression is upregulated after demethylation. Overexpression of GIPC2 in HL-60 cells can induce apoptosis by inhibiting the PI3K/AKT pathway. Conclusion: Our findings identify that GIPC2 is associated with the PI3K/AKT signaling pathway and may represent a potential therapeutic target and biomarker for the management of AML.
引用
收藏
页码：369 / 384
页数：16
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