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    A benzimidazolium salt induces apoptosis and arrests cells at sub-G1 phase in epithelial ovarian cancer cells
    (Springer, 2024) Akar, Sakine; Cakir, Mustafa; Ozkol, Halil; Akkoc, Senem; Ozdem, Berna
    BackgroundOvarian cancer, also known as a silent killer, is the deadliest gynecological cancer in women worldwide. Epithelial ovarian cancers constitute the majority of ovarian cancers, and diagnosis can be made in advanced stages, which greatly reduces the likelihood of treatment and lowers the survival rate. For the treatment of epithelial ovarian cancers, the search for synthetic agents as well as agents of natural origin continues. The effects of 1-(2-cyanobenzyl)-3-(4-vinylbenzyl)-1H-benzo[d]imidazole-3-ium chloride (BD), a benzimidazole derivative, were investigated on epithelial ovarian cancer cells.Methods and resultsIn our study, the effects of BD on proliferation, colony formation, cell death by apoptosis and the cell cycle in A2780 and A2780 Adriamycin (ADR) ovarian cancer cell lines were investigated. Proliferation was examined with cell viability analysis, colony formation and apoptosis with Annexin V staining and cell cycle analyses with PI staining, respectively. As a result of the analyses, BD inhibited cell proliferation and colony formation, induced apoptosis and cell death at 48 h in A2780 and A2780 ADR cells at 10.10 and 10.36 mu M concentrations, respectively. In addition, A2780 and A2780ADR cells were arrested in the Sub-G1 phase of the cell cycle.ConclusionsBD suppresses cancer cell progression by showing antiproliferative effects on ovarian cancer cells. Further analyses are required to determine the mechanism of action of this agent and to demonstrate its potential as a suitable candidate for the treatment of epithelial ovarian cancer.
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    A benzimidazolium salt induces apoptosis and arrests cells at sub-G1 phase in epithelial ovarian cancer cells (vol 51, 66, 2024)
    (Springer, 2024) Akar, Sakine; Cakir, Mustafa; Ozkol, Halil; Akkoc, Senem; Ozdem, Berna
    [Abstract Not Available]
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    Unveiling Benzoxazole-Substituted Thiazolyl-Pyrazole Derivatives Inducing Apoptosis by Targeting β-Tubulin and Caspase-3
    (Wiley-V C H Verlag Gmbh, 2025) Kuzu, Burak; Cakir, Mustafa; Acikgoz, Eda; Alagoz, Mehmet Abdullah
    In the present study, the biological activities of novel compounds (BP-1 to BP-6), designed as antitubulin agents, were systematically evaluated, with a particular focus on their effects on the triple-negative breast cancer cell line MDA-MB-231 and non-cancerous cell line MCF-10A. BP-2 and BP-6 demonstrated micromolar-range antiproliferative activity against MDA-MB-231 cancer cells, with IC50 values of 8 and 4 mu M, respectively, comparable to nocodazole (3 mu M), and showed selective cytotoxicity over normal MCF-10A cells, with selectivity indices of approximately 3.3 and 8. In vitro analyses revealed that BP-2 and more notably BP-6 significantly inhibited cell proliferation in a time- and dose-dependent manner, disrupted microtubule organization through the downregulation of beta-tubulin expression, and induced apoptosis, as evidenced by increased levels of Cleaved Caspase-3 and distinct apoptotic morphological changes. Among the tested compounds, BP-6 exhibited the most potent antiproliferative and proapoptotic activity, with an IC50 value close to that of NOC. Molecular docking supported these findings by showing strong binding affinities of BP-6 to both beta-tubulin and Caspase-3, indicating a dual-targeted mechanism. Furthermore, molecular dynamics simulations confirmed the stable binding and dynamic integrity of BP-6 within both beta-Tubulin and Caspase-3 targets, underscoring its potential as a robust candidate for anticancer drug development.