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    Apoptosis-inducing, anti-angiogenic and anti-migratory effects of a dinuclear Pd(II) complex on breast cancer: A promising novel compound
    (Academic Press Inc Elsevier Science, 2024) Genel, Merve Erkisa; Adacan, Kaan; Selvi, Selin; Kutucu, Deniz Erol; Uvez, Ayca; Armutak, Elif Ilkay; Sengul, Abdurrahman
    Because of the high mortality and morbidity rate of breast cancer, successful management of the disease requires synthesis of novel compounds. To this end, ongoing attempts to create new candidates include synthesis of multinuclear metal complexes. The high DNA binding affinity and cytotoxic activity of these complexes makes them promising as breast cancer treatments. This study investigated anti-growth/cytotoxic effect of the dinuclear Pd(II) complex on breast cancer cell lines (MCF-7, MDA-MB-231) using various methods of staining, flow cytometry, and immunoblotting. The study conducted colony formation, invasion, and migration assays were to assess the effect of the complex on metastasis. Increased caspase-3/7 levels and positive annexin V staining were observed in both cell lines, proving apoptosis. Altered TNFR1 and TRADD expression with caspase-8 cleavage followed by BCL-2 inactivation with loss of mitochondrial membrane potential confirmed the presence of apoptosis in MCF-7 and MDA-MB-231, regardless of p53 expression status. The results implied anti-migration properties. Finally, the study used the CAM assay to assess antiangiogenic properties and showed that the complex inhibited angiogenesis. The study concluded the dinuclear Pd(II) complex warrants further in vivo experiments to show its potential in the treatment of breast cancer.
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    Epibrassinolide impaired colon tumor progression and induced autophagy in SCID mouse xenograft model via acting on cell cycle progression without affecting endoplasmic reticulum stress observed in vitro
    (Elsevier Ltd, 2023) Obakan Yerlikaya, Pınar; Adacan, Kaan; Karatuğ Kaçar, Ayşe; Çöker Gürkan, Ajda; Arısan, Elif Damla
    Epibrassinolide is a member of brassinosteroids with a polyhydroxysteroid structure similar to steroid hormones of vertebrates. It was shown that EBR decreased cell proliferation and induced apoptosis in different colon cancer cell lines without exerting a cytotoxic effect in epithelial fetal human colon cells. This finding highlighted the potential of epibrassinolide in clinical therapeutic setup. In our previous studies, we showed that epibrassinolide was able to induce apoptosis via endoplasmic reticulum stress. Recently, we also showed that endoplasmic reticulum and apoptotic stresses can be prevented via autophagic induction in non-cancerous epithelial or aggressive forms of cancer cells. Therefore, here in this study, we evaluated the anti-tumoral effect of epibrassinolide as well as the autophagy involvement in the aggressive forms of colon cancer cell lines as well as in vivo SCID mouse xenograft colon cancer model for the first time. For this purpose, SCID mouse model was used for subcutaneous injection of colon cancer cells in matrigel formulation. We found that autophagy is induced in both in vitro and in vivo models. Following tumor formation, SCID mice were treated daily with increasing concentrations of epibrassinolide for two weeks. Our findings showed that EBR inhibited the volume and diameter of the tumor in a dose-dependent manner by causing cell cycle arrest. Therefore our data suggest that epibrassinolide exerts a cytostatic effect on the agrressive form of colon cancer model in vivo, without affecting endoplasmic reticulum stress and the induction of autophagy might have role in this effect of epibrassinolide. © 2023 Elsevier Ltd
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    Synthesis, Characterization and Apoptosis Capabilities of a Novel Naphthoquinone-Derived Compound in Triple-Negative Breast Cancer
    (Wiley-V C H Verlag Gmbh, 2023) Adacan, Kaan; Gokmen, Zeliha; Okan Akar, Remzi; Ozyildiz, Zeynep; Dincer, Hatice; Karakas, Didem; Ulukaya, Engin
    Breast cancer is the most frequently diagnosed cancer in women and the second leading cause of cancer-related deaths. Because triple-negative breast cancer (TNBC) is highly resistant to clinically employed drugs, developing new drugs and treatment approaches is imperative. Naphthoquinone compounds potentially induce cancer cell death, and their clinical derivatives have been widely used as medicines. This study presents the synthesis and structure of a newly substituted naphthoquinone compound, as determined by spectroscopic techniques, then assesses the compound's ability to induce cell death on the MDA-MB-231 cell line using SRB viability testing, flow cytometry, and Western Blotting. The study also examines the compound's inhibition of cell migration through a scratch assay. The study discovered that the compound demonstrated an antigrowth/cytotoxic impact at concentrations of 3.12 mu M and beyond. The cytotoxicity may have been caused by elevated reactive oxygen species, which resulted in DNA damage. The mode of cell death was apoptotic, confirmed by the translocation of phosphatidylserine, the activation of caspases, and the disruption of the mitochondrial membrane potential. The compound seems promising as a new anti-malignant agent to be used for the treatment of breast cancer and deserves further attention for proof-of-concept in animal studies. Breast cancer, the most prevalent female cancer and second-leading cancer cause of death, includes the aggressive TNBC variant. Naphthoquinone compounds show promise in TNBC treatment. Recent research reveals a novel naphthoquinone's potential in inducing apoptosis at concentrations >= 3.12 mu M, possibly via ROS elevation, DNA damage, and apoptotic cell death. Its ability to hinder cell migration suggests anti-metastatic properties. Yet, thorough research, including animal model validation and human safety and efficacy assessments, is crucial before deeming it a viable TNBC treatment.image