Gipc2 is a Tumor Suppressor Gene For Acute Myeloid Leukemia and Induces Apoptosis of Leukemia Cells by Regulating the Pi3K/Akt Pathway

Abstract

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.

Keywords::

• AML
• apoptosis
• GIPC2
• methylation
• PI3K/AKT

Supplementary data

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Financial & competing interests disclosure

This work was supported by grants from the National Natural Science Foundation of China (no. 81871725) and the Foundation of Department of Education of Liaoning Province (LJKZ0862). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Ethical conduct of research

The studies involving human subjects were reviewed and approved by the Ethical Committee of the First Affiliated Hospital of Dalian Medical University.

Additional information

Funding

This work was supported by grants from the National Natural Science Foundation of China (no. 81871725) and the Foundation of Department of Education of Liaoning Province (LJKZ0862). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.