AC024896.1/miR-363-3p Axis Regulates the Malignant Progression of Acute Myeloid Leukemia by Cuproptosis-Related Gene MYO1B

Abstract

Background

Acute myeloid leukemia (AML) is a hematological malignancy with poor patient prognosis. Cuprotosis is a newly discovered cell death that regulates the proliferation and progression of tumor cells. Long non-coding RNAs (lncRNAs) are key molecules and potential biomarkers for the diagnosis and treatment of various diseases. However, the effect of cuprotosis-associated lncRNAs on AML remains unclear.

Objective

The aim of this study was to investigate the relationship between the expression of cuprotosis-related gene and the prognosis of AML.

Methods

Consensus cluster analysis was performed on AML patients according to the cuprotosis-related gene expression matrix, and survival analysis and differential gene analysis were performed. Then lncRNA and miRNA related to AML tumor progression were screened according to univariate COX regression analysis. After that, Kaplan-Meier analysis, correlation analysis, and AUC curve were used to determine the ceRNA network that might regulate AML. The regulatory relationship of ceRNA was verified in AML cell lines by RT-qPCR and Western blotting.

Results

The AC024896.1/miR-363-3p axis drives MYO1B to promote the malignant progression of AML. First, a change in the expression of AC024896.1 and miR-363-3p can affect the proliferation of AML by regulating MYO1B. Mechanistically, AC024896.1 regulates the expression of MYO1B as the ceRNA of miR-363-3p. Moreover, the regulation of AC024896.1 in the malignant progression of AML depends partly on miR-363-3p.

Conclusion

In summary, our study reveals AC024896.1/miR-363-3p/MYO1B Axis in AML, which can be regarded as a new potential target for the diagnosis and treatment of AML.

Keywords:

• acute myeloid leukemia
• cuprotosis
• ceRNA network
• bioinformatics analysis

Data Sharing Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Ethical Approval

Our research followed the guidelines outlined by Article 32 of the “Measures for Ethical Review of Human Life Sciences and Medical Research” issued by the National Health Commission of the People’s Republic of China, which exempted the use of legally obtained public data from ethical review.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Additional information

Funding

The research received no external funding.