Evidence map›Paper›PMID 40754657›Full record

ArticleCancer reports (Hoboken, N.J.)2025

Targeting the mTOR Signaling Pathway Through miR-100 and miR-101 in De Novo Acute Myeloid Leukemia: Implications for Therapeutic Intervention.

Maryam Kargar, Mehdi Allahbakhshian Farsani, Javad Garavand, Mahnaz Gorji, Mohammad Rafiee, Seyed Sobhan Bahreiny, Mohammad Hossein Mohammadi

Abstract read
In one paragraph

Article in Cancer reports (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Maryam KargarDepartment of Laboratory Hematology and Blood Bank, School of Allied Medical Science, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0001-7922-7942
Mehdi Allahbakhshian FarsaniDepartment of Laboratory Hematology and Blood Bank, School of Allied Medical Science, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Javad GaravandDepartment of Laboratory Sciences, School of Allied Medical Sciences, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Mahnaz GorjiDepartment of Laboratory Hematology and Blood Bank, School of Allied Medical Science, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohammad RafieeDepartment of Medical Laboratory Sciences, School of Para Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
Seyed Sobhan BahreinyMedical Basic Sciences Research Institute, Physiology Research Center, Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Mohammad Hossein MohammadiHSCT Research Center, Laboratory Hematology and Blood Banking Department, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroribonucleic acid (MicroRNAs/miRNAs) play a significant role in cancer progression by changing cellular functions through the modulation of protein expressions. The potential of different miRNAs to alter the expression of the mammalian target of rapamycin (mTOR)/protein kinase B (PKB or AKT)/phosphatidylinositol-3-kinase (PI3K) signaling cascade, a key pathway in the progression of acute myeloid leukemia (AML), has been demonstrated across different types of cancers.

aimsThis study aims to explore the effects of miR-100 and miR-101 on the mTOR/AKT/PI3K signaling pathway in AML. METHODS AND

resultsInitially, we employed the TargetScan, miRDB, and miRanda databases to identify the target proteins of miR-100 and miR-101. Following a comprehensive analysis, we identified the mTOR/AKT/PI3K signaling pathway as a significant target for investigation in patients with AML. In this case-control study, the expression levels of miRNAs and genes were analyzed in 21 AML patients and 9 healthy controls using quantitative reverse transcription polymerase chain reaction (qRT-PCR). The results showed that miR-100 was significantly upregulated, while miR-101, mTOR, and PI3K were downregulated in AML patients. Correlation analysis revealed a negative relationship for miR-100 and a positive one for miR-101 with mTOR, but no significant correlation with AKT1 and PI3K genes.

conclusionThese findings suggest that both miR-100 and miR-101 act as tumor suppressors via the mTOR/AKT/PI3K signaling pathway, highlighting their potential as therapeutic targets in AML.

Indexed as

Leukemia, Myeloid, AcuteMicroRNAsTOR Serine-Threonine KinasesAdultAgedCase-Control StudiesFemaleGene Expression Regulation, LeukemicHumansMaleMiddle AgedProto-Oncogene Proteins c-aktSignal TransductionYoung AdultMicroRNAsMIRN100 microRNA, humanMIRN101 microRNA, humanMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinasesacute myeloid leukemiamicroRNA‐100microRNA‐101mTOR/AKT/PI3K pathway

Identifiers

PMID40754657
PMCPMC12318680

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.