Enhanced Expression of miR-638-5p May Suppress Acute Myeloid Leukemia in vitro Cell Proliferation Through PGK1 and PIM1

Objective: miR-638-5p is a crucial tumor suppressor miRNA in several cancer types including, Acute Myeloid Leukemia (AML). This study aimed to analyze the role of miR-638-5p and its potential target genes in HL-60 and NB4 acute promyelocytic leukemia cell lines using in vitro method. Method: After the miR-638-5p mimic transfection into AML cells, the effect on cell viability was examined by the WST-8 method, and the effect on apoptosis was measured via the Caspase-3 quantification method. In silico tools such as miRWalk, miRDB, and miRTarBase were used to select the possible target genes of miR-638-5p. The expression levels of selected genes were investigated by qRT-PCR. The overall survival (OS) rate of AML patients was explored via the BloodSpot database, the Enrichr tool was used for enrichment analysis, and correlation analysis was performed using the Correlation AnalyzeR tool. Results: Decreased proliferation and increased apoptosis were determined in miR-638-5p mimic transfected cells compared to the controls. MECP2, PIM1, MEF2C, PGK1, and SPAG1 genes were selected as the potential targets of miR-638-5p for in vitro study. PGK1 and PIM1 expression levels were significantly suppressed in cells transfected with the miR-638-5p mimic. The OS investigation revealed that overexpression of MECP2, MEF2C, and PGK1 does not affect the survival of AML patients; however, overexpression of SPAG1 and PIM1 has a detrimental effect on AML survival. Also, a positive correlation was detected between PIM1 and PGK1 genes via enrichment analysis. Conclusion: miR-638-5p may contribute to AML pathogenesis by targeting the PGK1 and PIM1 genes, and this situation may indicate its potential as a biomolecule for regulating cell proliferation in AML cells.

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Publication Details

Journal
Konuralp Tıp Dergisi
Published
2025-03-27
DOI
https://doi.org/10.18521/ktd.1600640
Primary Topic
Cancer Mechanisms and Therapy
Type
article
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article

Enhanced Expression of miR-638-5p May Suppress Acute Myeloid Leukemia in vitro Cell Proliferation Through PGK1 and PIM1

Şükrü Öztürk, Murat Kaya, İlknur Süer, Simge Özkaynak
Konuralp Tıp Dergisi
Cancer Mechanisms and Therapy
article

Enhanced Expression of miR-638-5p May Suppress Acute Myeloid Leukemia in vitro Cell Proliferation Through PGK1 and PIM1

Şükrü Öztürk, Murat Kaya, İlknur Süer, Simge Özkaynak
article en

Abstract

Objective: miR-638-5p is a crucial tumor suppressor miRNA in several cancer types including, Acute Myeloid Leukemia (AML). This study aimed to analyze the role of miR-638-5p and its potential target genes in HL-60 and NB4 acute promyelocytic leukemia cell lines using in vitro method. Method: After the miR-638-5p mimic transfection into AML cells, the effect on cell viability was examined by the WST-8 method, and the effect on apoptosis was measured via the Caspase-3 quantification method. In silico tools such as miRWalk, miRDB, and miRTarBase were used to select the possible target genes of miR-638-5p. The expression levels of selected genes were investigated by qRT-PCR. The overall survival (OS) rate of AML patients was explored via the BloodSpot database, the Enrichr tool was used for enrichment analysis, and correlation analysis was performed using the Correlation AnalyzeR tool. Results: Decreased proliferation and increased apoptosis were determined in miR-638-5p mimic transfected cells compared to the controls. MECP2, PIM1, MEF2C, PGK1, and SPAG1 genes were selected as the potential targets of miR-638-5p for in vitro study. PGK1 and PIM1 expression levels were significantly suppressed in cells transfected with the miR-638-5p mimic. The OS investigation revealed that overexpression of MECP2, MEF2C, and PGK1 does not affect the survival of AML patients; however, overexpression of SPAG1 and PIM1 has a detrimental effect on AML survival. Also, a positive correlation was detected between PIM1 and PGK1 genes via enrichment analysis. Conclusion: miR-638-5p may contribute to AML pathogenesis by targeting the PGK1 and PIM1 genes, and this situation may indicate its potential as a biomolecule for regulating cell proliferation in AML cells.

Konuralp Tıp DergisiVol. 17(1)
Istanbul University (TR)
Openalex Percentile: Top 61%
Cancer Mechanisms and Therapy
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