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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
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    Targeting Periostin Expression Makes Pancreatic Cancer Spheroids More Vulnerable to Natural Killer Cells
    (Mdpi, 2023) Karakas, Didem; Erkisa, Merve; Akar, Remzi Okan; Akman, Gizem; Senol, Ezgi Yudum; Ulukaya, Engin
    Pancreatic cancer (PaCa) characteristically has a dense tumor microenvironment, which results in poor patient prognosis. Pancreatic stellate cells (PSCs) are the most abundant cells in the PaCa microenvironment and the principal source of collagen. Periostin, a matricellular protein, is produced specifically by PSCs and promotes the aggressiveness of PaCa cells by facilitating extracellular collagen assembly. Here, we aimed to decrease extracellular collagen assembly by suppressing periostin, thereby increasing the cytotoxic activity of natural killer (NK) cells. Periostin expression was suppressed in PSCs (called PSC-P) using CRISPR-Cas9. PaCa cells (BxPC-3) were co-cultured with PSC and PSC-P cells in a 3D environment to form tumor spheroids mimicking the tumor microenvironment. The extracellular collagen production of spheroids was evaluated by Masson's trichrome staining. The cytotoxic activity of NK-92 cells was analyzed by flow cytometry and confocal microscopy via CD107a staining. Cell death in BxPC-3 cells was evaluated by measuring Annexin-V and PI positivity using flow cytometry. As a result, periostin suppression decreased extracellular collagen and increased the infiltration of NK-92 cells into spheroids, and induced cell death in PaCa cells. In conclusion, we suggest that periostin might be a therapeutic target for PaCa and further analysis is warranted using in vivo models for proof-of-concept.