Evidence mapPaperPMID 42461339Full record

ArticleMolecular biology reports2026

Agomelatine versus gefitinib against HepG2 cells: Modulating PI3K/AKT and MAPK/RAF1/c-FOS pathways.

Heba M Abd El Kareem, Sara F Saadawy, Mai M ELdaly, Yousef Al-Saraireh, Heba A Hassan

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Heba M Abd El KareemDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, Benha University, Benha, 13511, Egypt.
Sara F SaadawyMedical Biochemistry Department, Faculty of Medicine, Zagazig University, Zagazig, 44519, Egypt.
Mai M ELdalyMedical Biochemistry Department, Faculty of Medicine, Zagazig University, Zagazig, 44519, Egypt.
Yousef Al-SarairehPharmacology Department, Faculty of Medicine, Mutah University, P.O. Box 7, Al-Karak, 61710, Jordan.
Heba A HassanPharmacology Department, Faculty of Medicine, Mutah University, P.O. Box 7, Al-Karak, 61710, Jordan. HAHanafi@medicine.zu.edu.eg.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is the predominant form of cancer globally, characterized by a dismal prognosis and few treatment options. Agomelatine (AGO) acts as a melatonin receptor agonist and a 5-HT2C receptor antagonist, suggesting its potential anticancer efficacy across diverse cancer types.

aimThis study aims to assess the effects of AGO and gefitinib (GEF) on apoptosis, cell cycle, and caspase expression, and to examine their implications for the PI3K/AKT and MAPK/ERK pathways.

methodsThe concentrations of AGO and GEF were altered in the cells. MTT tests (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) were used. A flow cytometry experiment was conducted after a single dose of AGO and GEF. The RT-qPCR test was used to assess the expression levels of caspases 8 and 9, as well as the PI3K/AKT and MAPK/RAF/c-FOS genes.

resultsAGO and GEF increased caspase expression, reduced cell viability, and induced apoptosis while inhibiting the expression of PI3K/AKT and MAPK/ERK genes.

conclusionOur results demonstrated that both AGO and GEF impeded HCC progression by enhancing apoptosis and caspase expression while modulating the PI3K/AKT and MAPK/RAF/c-FOS signaling pathways, suggesting that AGO and GEF may serve as effective therapeutic options for HCC, with gefitinib exhibiting greater potential as an anticancer agent.

Indexed as

AcetamidesCarcinoma, HepatocellularGefitinibLiver NeoplasmsAntineoplastic AgentsApoptosisCell CycleCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHep G2 CellsHumansMAP Kinase Signaling SystemNaphthalenesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAcetamidesagomelatineAntineoplastic AgentsGefitinibNaphthalenesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-fosAgomelatineCytotoxicityGefitinibGene studiesHepatocellular carcinomaMTT

Identifiers

PMID42461339

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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.