HCP5, as the sponge of miR-1291, facilitates AML cell proliferation and restrains apoptosis via increasing PIK3R5 expression

Yan Liu,Xue-Bing Jing,Zhen-Cheng Wang,Qing-Kun Han

doi:10.1186/s40246-021-00340-5

Abstract

BackgroundAcute myeloid leukemia (AML) is recognized as a hematological neoplasm with heterogenetic cytology and short-term outcome. HCP5 has been proven to be related with the pathogenesis of AML. However, the underlying mechanism of HCP5 in AML remains unclear.MethodsClinical profiles of AML patients were downloaded from TCGA and GTEx databases. LncBase and TargetScan online tools were utilized to predict potential targets, and dual-luciferase reporter assay was performed to verify the association between miR-1291 and HCP5 or PIK3R5. Cell Counting Kit 8 and flow cytometry tests were implemented to evaluate the effects of HCP5/miR-1291/PIK3R5 axis in AML cells. Quantitative RT-PCR and Western blot were conducted to detect the expression levels of genes.ResultsHCP5 and PIK3R5 were significantly increased in AML tissue samples compared with healthy controls. HCP5 facilitated AML cells viability and inhibited apoptosis. There was a positive relationship between HCP5 and PIK3R5, but miR-1291 negatively regulated PIK3R5. Overexpression of PIK3R5 enhanced the promoting effect of HCP5 in the development of AML, while weakened the suppression of miR-1291 to AML progression.ConclusionOur findings manifested that HCP5 was remarkably upregulated in AML and upregulated HCP5 promoted the malignant behaviors of AML cells by mediating miR-1291/PIK3R5 axis, which would provide a new insight for the treatment of AML.

Highlights

Acute myeloid leukemia (AML) is recognized as a hematological neoplasm with heterogenetic cytology and short-term outcome
Our findings manifested that histocompatibility leukocyte antigen (HLA) complex P5 (HCP5) was remarkably upregulated in AML and upregulated HCP5 promoted the malignant behaviors of AML cells by mediating miR-1291/Phosphoinositide-3-Kinase Regulatory Subunit 5 (PIK3R5) axis, which would provide a new insight for the treatment of AML
PIK3R5 is positively associated with HCP5, and their expressions are significantly increased in AML To explore the specific mechanism of AML and identify the potential biomarker genes, we downloaded the RNA-Seq and clinical profiles of LAML from TCGA and GTEx database, including 151 tumor samples and 70 normal human bone marrow cell samples as the control group

Summary

Introduction

Acute myeloid leukemia (AML) is recognized as a hematological neoplasm with heterogenetic cytology and short-term outcome. As an aggressive hematological and heterogeneous malignancy, acute myeloid leukemia (AML) is the most common disease related with abnormally increased proliferation and impaired ability to differentiate of myeloid progenitor cells [1]. Liu et al Human Genomics (2021) 15:38 is emerging evidence that lncRNAs function as key regulators for the differentiation and maturation of myeloid, participating in regulating AML cells viability and apoptosis. Downregulation of HOTAIRM1 promoted Ara-C-stimulated attenuation of cell proliferation and increase of apoptosis capacity [6]. Another lncRNA UCA1 has been reported to regulate cell viability of AML cells and cell cycle [7]. The complex lncRNA/miRNA/mRNA network involved with HCP5 in AML still remains elusive

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Discussion

Conclusion