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Up-Regulation of miR-625-5p Correlates with Suppressed Sox2, Increased Apoptosis, and Cell Cycle Arrest via The

Kangup Steven Kereka1, Seyed Hadi Mousavi1, Shaban Alizadeh1

  • 1Department of Haematology and Blood Transfusion, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran.

International Journal of Hematology-Oncology and Stem Cell Research
|December 20, 2024
PubMed
Summary

MicroRNA-625 (miR-625) up-regulation in Acute Myeloid Leukemia (AML) cells reduced proliferation and induced apoptosis by targeting Sox2. This suggests miR-625 as a potential therapeutic strategy for AML.

Keywords:
Acute myeloid leukaemiaPI3K/AKT signaling pathwayProliferationSox2miR-625

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Area of Science:

  • Molecular Biology
  • Oncology
  • Gene Regulation

Background:

  • MicroRNA-625 (miR-625) and Sox2 gene expression are altered in various cancers.
  • The phosphatidylinositol 3'-kinase/protein kinase B (PI3K/Akt) pathway is implicated in hematological malignancies like Acute Myeloid Leukemia (AML).
  • Aberrant miR-625 and Sox2 expression are observed in cancers, with PI3K/Akt pathway involvement in AML.

Purpose of the Study:

  • To investigate the impact of miR-625 up-regulation on proliferation, apoptosis, and cell cycle in KG-1 cells.
  • To determine if miR-625 targets the Sox2 gene via the Akt signaling pathway and affects cell cycle regulators (p21, p27, cyclin E).

Main Methods:

  • KG-1 cell line transfection with miR-625 or a control plasmid using electroporation.
  • Flow cytometry analysis for cell cycle, proliferation, and apoptosis assessment.
  • Quantitative real-time PCR (qRT-PCR) for validating gene expression levels of miR-625, Sox2, p21, p27, and cyclin E.

Main Results:

  • Transfection with miR-625 significantly decreased proliferation and increased apoptosis in KG-1 cells.
  • miR-625 induced cell cycle arrest.
  • Upregulation of miR-625 led to decreased Sox2, p21, and cyclin E, with increased p27 expression (P < 0.05).

Conclusions:

  • MiR-625 demonstrates potential as a therapeutic agent for Acute Myeloid Leukemia.
  • Further research is warranted to explore the therapeutic applications of miR-625 in AML treatment.