Evidence map›Paper›PMID 41233610›Full record

ArticleIrish journal of medical science2026

The effect of PARP and PLK1 dual inhibition on the expression of important protein signaling pathways, DNA damage, and molecular docking scores against MCF-7 and MDA-MB-231 breast cancer cell lines.

Özlem Gök, Abdullah Aslan, Mehmet Kadir Erdoğan, Harun Uslu, Yusuf Toy, Can Ali Ağca, Seda Beyaz, Ramazan Gundogdu

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Article in Irish journal of medical science, 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

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

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

8 authors.

Özlem GökFaculty of Science, Department of Biology-Molecular Biology and Genetics, Firat University, Elazig, Turkey.
Abdullah AslanFaculty of Science, Department of Biology-Molecular Biology and Genetics, Firat University, Elazig, Turkey. aaslan@firat.edu.tr.
Mehmet Kadir ErdoğanFaculty of Science, Department of Molecular Biology and Genetics, Bingol University, Bingol, Turkey.
Harun UsluFaculty of Pharmacy, Department of Pharmaceutical Chemistry, Firat University, Elazig, Turkey.
Yusuf ToyFaculty of Science, Department of Molecular Biology and Genetics, Bingol University, Bingol, Turkey.
Can Ali AğcaFaculty of Science, Department of Molecular Biology and Genetics, Bingol University, Bingol, Turkey.
Seda BeyazFaculty of Science, Department of Biology-Molecular Biology and Genetics, Firat University, Elazig, Turkey.
Ramazan GundogduDepartment of Pharmacy Services, Bingol University, Vocational School of Health Services, Bingol, Turkey. rgundogdu@bingol.edu.tr.

Funding

Bingöl University Scientific Research Projects BAP-SHMYO.2019.00.002Council of Higher Education (COHE) 100/2000 biotechnology priority area doctoral project 100/2000Firat University Scientific Research Projects Management Unit FF.21.22Scientific and Technological Research Council of Turkey (TÜBİTAK) Scientist Support Programs Directorate (BİDEB) 2211-A
6 · The paper itself

Abstract

backgroundSmall molecule PARP inhibitors, such as olaparib, have been developed as part of personalized cancer treatment strategies.

aimThis study investigated the synthetic lethality between the PARP enzyme in breast cancer cell lines.

methodsThe anti-cancer effects of combining the PARP inhibitor olaparib with the small molecule PLK1 inhibitor BI-2536 on MCF-7 and MDA-MB-231 breast cancer cells were assessed through in vitro cell viability (MTT) and clonogenic cytotoxicity analyses. The impact of olaparib and BI-2536 treatment on cell cycle and DNA damage response proteins was analyzed using Western blotting. BRCA2 expression was silenced using RNA interference technology, and the manipulation of BRCA2 gene expression in MCF-7 breast cancer cells was confirmed by Western blotting. Cell viability and colony survival were evaluated in BRCA2-effective and BRCA2-defective MCF-7 cells. Additionally, molecular docking analyses provided insights into the functioning of protein signaling pathways.

resultsOur results indicate that the combined treatment with olaparib and BI-2536 significantly reduces the viability of MCF-7 and MDA-MB-231 breast cancer cells and inhibits their colony formation ability. This combination therapy demonstrated a synergistic cytotoxic effect, causing potentiated DNA damage induction in these breast cancer cells compared to individual treatments.

conclusionsThe increased expression of PLK1, p53, p21, γH2AX, Nrf-2, cyclin E, A, and B1, along with the decreased expression of HER-2, NF-κB, and cyclin D1 in breast cancer cells, suggests that PLK1 inhibition can enhance the efficacy of PARP inhibitors.

Indexed as

Breast NeoplasmsCell Cycle ProteinsDNA DamagePhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene ProteinsPteridinesBRCA2 ProteinCell Line, TumorCell SurvivalFemaleHumansMCF-7 CellsMolecular Docking SimulationBI 2536BRCA2 ProteinCell Cycle ProteinsolaparibPhthalazinesPiperazinesPolo-Like Kinase 1Poly(ADP-ribose) Polymerase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene ProteinsPteridinesBI-2536DNA damageMCF-7MDA-MB-231Olaparib

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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.