Evidence map›Paper›PMID 39903385›Full record

ArticleMolecular biology reports2025

Comparative effects of arsenic trioxide and chemotherapy on Chk1 and CDC25 gene expression in gastric cancer cells AGS and MKN45: a potential therapeutic strategy.

Shadi Babaei, Mohsen Nikbakht, Ahmad Majd, Seyed Asadoullah Mousavi

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

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4citing papers in PubMed
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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

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Shadi BabaeiDepartment of Biology, North Tehran Branch, Islamic Azad University, Tehran, Iran.
Mohsen NikbakhtResearch Institute for Oncology, Hematology and Cell Therapy, Tehran University of Medical Sciences, Tehran, Iran. m-nikbakht@sina.tums.ac.ir.
Ahmad MajdDepartment of Biology, North Tehran Branch, Islamic Azad University, Tehran, Iran.
Seyed Asadoullah MousaviResearch Institute for Oncology, Hematology and Cell Therapy, Tehran University of Medical Sciences, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGastric cancer (GC) remains a significant global health burden, particularly in East Asia, where it is a leading cause of cancer-related morbidity and mortality. Despite advancements in chemotherapy, the development of chemoresistance continues to undermine the efficacy of standard treatments such as Docetaxel and Oxaliplatin. Arsenic trioxide (ATO) has emerged as a potential therapeutic agent capable of overcoming resistance by targeting DNA repair mechanisms, particularly through the downregulation of Checkpoint Kinase 1 (Chk1). This study investigates the cytotoxic effects of ATO and its capacity to enhance chemotherapy efficacy in GC cells.

methodsAGS and MKN-45 gastric cancer cell lines were exposed to ATO, Docetaxel, Oxaliplatin, and their combinations. Cell viability was assessed via the MTT assay, while Chk1 and CDC25 expressions at the mRNA and protein levels was analyzed using real-time PCR and Western blotting. Statistical analyses were performed using ANOVA and Tukey's post hoc test.

resultsThe MTT assay revealed significant dose- and time-dependent reductions in cell viability, with combination treatments achieving the most pronounced effects. The greatest cytotoxicity was observed with 4 µM ATO combined with 2500 µM Docetaxel or 100 µM Oxaliplatin, showing a high level of statistical significance (p < 0.0001). Additionally, ATO monotherapy significantly downregulated Chk1 and CDC25 expressions (p < 0.05), while its combination with chemotherapeutic agents further enhanced Chk1 and CDC25 suppressions, with ATO-Docetaxel demonstrating the most pronounced effect (p < 0.01).

conclusionsThese findings highlight ATO's potential to sensitize GC cells to chemotherapy by impairing DNA repair mechanisms and inducing synergistic cytotoxicity. ATO holds promise as an adjuvant therapeutic agent for overcoming chemoresistance in gastric cancer.

Indexed as

Arsenic Trioxidecdc25 PhosphatasesCheckpoint Kinase 1Stomach NeoplasmsAntineoplastic AgentsCell Line, TumorCell SurvivalDocetaxelDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansOrganoplatinum CompoundsOxaliplatinOxidesTaxoidsAntineoplastic AgentsArsenic Trioxidecdc25 PhosphatasesCheckpoint Kinase 1CHEK1 protein, humanDocetaxelOrganoplatinum CompoundsOxaliplatinOxidesTaxoidsArsenic trioxideCDC25ChemoresistanceChk1DNA damage responseDocetaxelGastric cancerOxaliplatin

Identifiers

PMID39903385

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