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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
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Targeting the mTOR Signaling Pathway Through miR-100 and miR-101 in De Novo Acute Myeloid Leukemia: Implications for

Maryam Kargar1, Mehdi Allahbakhshian Farsani1,2, Javad Garavand3

  • 1Department of Laboratory Hematology and Blood Bank, School of Allied Medical Science, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Cancer Reports (Hoboken, N.J.)
|August 3, 2025
PubMed
Abstract

Insights

MicroRNAs (miRNAs) miR-100 and miR-101 show potential as tumor suppressors in acute myeloid leukemia (AML). They influence the mammalian target of rapamycin (mTOR)/AKT/phosphatidylinositol-3-kinase (PI3K) pathway, suggesting novel therapeutic targets for AML treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • MicroRNAs (miRNAs) regulate gene expression and are implicated in cancer progression.
  • The mammalian target of rapamycin (mTOR)/protein kinase B (AKT)/phosphatidylinositol-3-kinase (PI3K) pathway is crucial in acute myeloid leukemia (AML) development.
  • Specific miRNAs can modulate the mTOR/AKT/PI3K pathway in various cancers.

Purpose of the Study:

  • To investigate the impact of miR-100 and miR-101 on the mTOR/AKT/PI3K signaling pathway in AML.
  • To determine the expression levels of miR-100, miR-101, and key pathway components in AML patients.

Main Methods:

  • Bioinformatic databases (TargetScan, miRDB, miRanda) were used to predict miRNA targets.
  • Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was employed to measure miRNA and gene expression.
  • A case-control study design included 21 AML patients and 9 healthy controls.

Main Results:

  • miR-100 was significantly upregulated in AML patients.
  • miR-101, mTOR, and PI3K were significantly downregulated in AML patients.
  • miR-100 showed a negative correlation with mTOR, while miR-101 exhibited a positive correlation with mTOR.

Conclusions:

  • miR-100 and miR-101 function as tumor suppressors in AML by affecting the mTOR/AKT/PI3K pathway.
  • These miRNAs represent potential therapeutic targets for AML treatment.
Keywords:
acute myeloid leukemiamTOR/AKT/PI3K pathwaymicroRNA‐100microRNA‐101

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