Evidence map›Paper›PMID 40917720›Full record

ArticleBiochemistry and biophysics reports2025

Inhibition of PI3K/AKT/mTOR signaling enhances autophagy in HL-60 acute myeloid leukemia cells: An integrative bioinformatic and in vitro study.

Mohammad Malekan, Armin Dozandeh-Jouybari, Nazanin Joudaki, Mehdi Ahangari, Reza Valadan, Hossein Asgarian-Omran, Saeid Taghiloo

Abstract read
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Article in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

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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.

Mohammad MalekanStudent Research Committee, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Armin Dozandeh-JouybariDepartment of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Nazanin JoudakiStudent Research Committee, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Mehdi AhangariStudent Research Committee, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Reza ValadanDepartment of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Hossein Asgarian-OmranDepartment of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Saeid TaghilooDepartment of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Acute myeloid leukemia (AML) involves uncontrolled proliferation of myeloid progenitor cells and carries a poor prognosis. The PI3K/AKT/mTOR pathway plays a key role in AML pathogenesis by regulating cancer cell proliferation and survival. This study investigates the effects of inhibiting the PI3K/AKT/mTOR pathway on autophagy in AML cell lines, aiming to support targeted therapy development that modulates autophagy. Methods: Gene expression and prognostic significance of PI3K/AKT/mTOR and autophagy-related genes in AML were evaluated using Enricher, GEPIA2, and Human Protein Atlas databases. HL-60 cells were treated with Idelalisib, MK-2206, and Everolimus, selective PI3K, AKT, and mTOR inhibitors, either individually or in combination. Autophagy gene expression ( Result: Bioinformatic analysis revealed that autophagy genes are associated with PI3K/AKT/mTOR pathway in AML. We observed that HL-60 AML cell lines treated with PI3K/AKT/mTOR inhibitors exhibited significant enhancement in the expression of key autophagy-related genes, including Conclusion: PI3K/AKT/mTOR inhibitors significantly induce autophagy-related gene expression in AML cells. These findings support combining such inhibitors with autophagy modulators as a potential strategy to improve AML treatment outcomes.

Indexed as

Acute myeloid leukemiaAutophagyEverolimusIdelalisibMK 2206PI3K/AKT/mTOR

Identifiers

PMID40917720
PMCPMC12409794

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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 OpenQuestion graph.