[
    {
        "id": "osp-2815",
        "type": "article-journal",
        "title": "E2F-1–Akt1 Interaction as Precursor to Cisplatin-induced Apoptosis in Triple-negative Breast Cancer Cells",
        "author": [
            {
                "family": "Al-Jaaidi",
                "given": "Samiya"
            },
            {
                "family": "Al-Dhahli",
                "given": "Buthaina"
            },
            {
                "family": "Al Sibani",
                "given": "Asma"
            },
            {
                "family": "Al Harthi",
                "given": "Thraia"
            },
            {
                "family": "Al Ghafri",
                "given": "Hajar"
            },
            {
                "family": "Al-Bahlani",
                "given": "Shadia"
            }
        ],
        "URL": "https://omanscience.com/en/articles/e2f-1-akt1-interaction-as-precursor-to-cisplatin-induced-apoptosis-in-triple-negative-breast-cancer-cells",
        "language": "en",
        "issued": {
            "date-parts": [
                [
                    2025
                ]
            ]
        },
        "container-title": "Oman Medical Journal",
        "DOI": "10.5001/omj.2025.41",
        "publisher": "Oman Medical Specialty Board",
        "ISSN": "1999-768X",
        "abstract": "Objectives: We aimed to investigate the expression levels and interaction between E2F-1 and Akt1 in triple-negative breast cancer (TNBC) cells, and whether cis-diamminedichloroplatinum(II) (cisplatin) could influence such an interaction. Methods: A batch of MDA-MB-321 breast cancer cells were treated with increasing concentrations of cisplatin (2.5–40 μM) for 24 hours. Additional cells from the same source were used for control experiments. Cisplatin-induced apoptosis was confirmed biochemically using cleaved polymerase and flow cytometry analysis, and morphologically using hematoxylin and eosin staining, Hoechst staining, and scanning electron microscopy. Caspase-3 cleavage, an indicator of apoptotic induction, was measured by immunofluorescence. A western blot test was used to investigate the effects of cisplatin on E2F-1 and Akt1 expressions, while their co-localization and interaction were detected using immunofluorescence and immunoprecipitation, respectively. Results: A western blot analysis revealed an increase in E2F-1 and a decrease in Akt1 expression with increasing concentration of cisplatin, compared to untreated cells. Merged E2F-1 and Akt1 immunosignals observed by immunofluorescence demonstrated that cisplatin-treated cells exhibited co-localization of immunosignals in clusters and with increased intensity in the cytoplasm. Immunoprecipitation and western blot analysis results further confirmed the association between E2F-1 and Akt1, indicating a potential interaction between the two proteins in MDA-MB-231 cells. Conclusions: Our findings suggest a potential interaction between E2F-1 and Akt1, which in turn could be the precursor for the cisplatin-induced apoptosis in TNBC cells. Further studies are needed to determine whether this interaction occurs directly or via an intermediate protein."
    }
]