Evidence map›Paper›PMID 41779250›Full record

ArticleMolecular biology reports2026

BET inhibition enhances temozolomide sensitivity in cervical cancer cells through ALDH suppression and epigenetic reprogramming.

Kemal Eker, Maryam Sabour Takanlou, Leila Sabour Takanlou, Arman Rostamlou, Cigir Biray Avci

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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. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

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4 · The record

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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

5 authors.

Kemal EkerFaculty of Medicine, Ege University, Izmir, Turkey.ORCID http://orcid.org/0009-0008-4916-5128
Maryam Sabour TakanlouDepartment of Medical Biology, Faculty of Medicine, Ege University, Bornova, Izmir, 35100, Turkey.ORCID http://orcid.org/0000-0002-1590-4833
Leila Sabour TakanlouDepartment of Medical Biology, Faculty of Medicine, Ege University, Bornova, Izmir, 35100, Turkey.ORCID http://orcid.org/0000-0002-6361-7150
Arman RostamlouDepartment of Medical Biology, Faculty of Medicine, Ege University, Bornova, Izmir, 35100, Turkey.ORCID http://orcid.org/0009-0001-4336-562X
Cigir Biray AvciDepartment of Medical Biology, Faculty of Medicine, Ege University, Bornova, Izmir, 35100, Turkey. cbavci@gmail.com.ORCID http://orcid.org/0000-0001-8251-4520

Funding

Ege Üniversitesi TLP-2021-23416
6 · The paper itself

Abstract

backgroundCervical cancer remains one of the most prevalent gynecological malignancies worldwide, and therapeutic resistance continues to limit the effectiveness of current treatment strategies. Aldehyde dehydrogenase 1 (ALDH1) has been associated with chemoresistance and cellular stress responses in cervical cancer, while bromodomain and extraterminal (BET) proteins have emerged as regulators of transcriptional and epigenetic programs involved in tumor progression. In this study, we investigated whether BET inhibition by JQ1 modulates cellular responses to temozolomide (TMZ) in cervical cancer cells.

methodsHeLa cells were treated with JQ1, TMZ, or TMZ + JQ1, alongside untreated controls. Cell viability and proliferation were evaluated using the WST-1 assay, and apoptotic cell death was assessed by Annexin V/propidium iodide staining and flow cytometry. Oxidative stress related changes were examined using malondialdehyde (MDA) measurements. Transcriptional alterations associated with epigenetic regulation were explored using the Human Epigenetic Chromatin Modification Enzymes RT² Profiler PCR Array and targeted RT-qPCR analysis of BET family members and ALDH isoforms.

resultsJQ1 and TMZ treatments reduced HeLa cell proliferation in a dose-dependent manner, with the combined treatment producing a modest additional antiproliferative effect compared with single agents. Flow cytometric analysis demonstrated increased apoptotic fractions in treated cells, particularly following combined exposure. MDA levels were reduced in JQ1-treated and JQ1 + TMZ treated cells, indicating altered oxidative stress status. Gene expression profiling revealed differential regulation of multiple chromatin-modifying enzymes involved in acetylation- and methylation-related pathways, while RT-qPCR analysis demonstrated coordinated transcriptional downregulation of BET family members and ALDH isoforms following combined treatment.

conclusionThis study demonstrates that BET inhibition by JQ1 influences cellular sensitivity to TMZ and is associated with altered oxidative stress parameters and transcriptional reprogramming of epigenetic regulators in cervical cancer cells. While further protein-level and functional validation is required to establish causal mechanisms, these findings support the potential of BET-targeted strategies to modulate therapeutic responses in cervical cancer.

Indexed as

Epigenesis, GeneticProteinsRetinal DehydrogenaseTemozolomideUterine Cervical NeoplasmsAldehyde Dehydrogenase 1 FamilyApoptosisAzepinesBromodomain Containing ProteinsCell Line, TumorCell ProliferationCell SurvivalDacarbazineDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticAldehyde Dehydrogenase 1 FamilyALDH1A1 protein, humanAzepinesbromodomain and extra-terminal domain protein, humanBromodomain Containing ProteinsDacarbazine(+)-JQ1 compoundProteinsRetinal DehydrogenaseTemozolomideTriazolesApoptosisCervical cancerEpigenetic regulationJQ1Oxidative stressTemozolomide

Identifiers

PMID41779250

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.