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Öğe [1]Vitamin B12 Enhances Cisplatin Efficacy via Apoptosis and MAPK/ERK1-2, P38, PARP-1 Modulation in Prostate Cancer(Yuzuncu Yil Universitesi Tip Fakultesi, 2025) Evyapan, Gulsah; Ozdem, Berna; Tekedereli, IbrahimIntroduction: Prostate cancer (PC) is the most common malignancy among men and remains a major cause of cancer-related mortality worldwide. Cisplatin is a widely used chemotherapeutic agent in cancer treatment. Vitamin B12 has been shown to play a role i n enhancing the efficacy of certain cancer drugs when used in combination therapies. This study investigates the antitumor effects and mechanisms of action of B12 and Cisplatin combination therapy in prostate cancer cells. Materials and Methods: The clonogenic assay was used to determine the fraction of surviving cells after treatment. The MTS assay and flow cytometry were performed to assess the impact of B12 and Cisplatin on cell proliferation and apoptosis, while Western bl ot analysis was used to examine the expression of key signaling proteins involved in these processes. Results: Our results revealed that the combination treatment of B12 and Cispalatin significantly inhibited the proliferation and viability o f the PC cell line. Also, clonogenic assay indicated that B12 and Cisplatin combination treatment inhibited the colony formation. Moreover, the combined treatment showed a 2.3-fold increase in P38 and a 1.8-fold increase in PARP-1 protein expression compared to control. In addition, MAPK/ERK1-2 and Bcl-2 protein expression were significantly reduced by approximately 40% and 45% respectively in the combination treatment. Conclusion: Our findings suggest that the combination of B12 and Cisplatin enhances the antitumor effects of Cisplatin by promoting apoptosis and modulating key signaling pathways, including P38, PARP-1, and MAPK/ERK1-2. These findings, supported by significant reductions in cell viability (up to 50%), suggest a promising role for B12 and Cisplatin combination therapy. Further in vivo and clinical studies are warranted to validate these preliminary in vitro findings. © 2025, Yuzuncu Yil Universitesi Tip Fakultesi. All rights reserved.Öğe Inhibition of Autophagy by ATG5 siRNA Transfection Enhances Anti-cancer Effects of Gum Arabic, Promotes Oxidative Stress-Mediated Apoptosis and Affects DNA Damage and Mitochondrial Membrane Potential in Ovarian Cancer Cells(Springernature, 2026) Evyapan, Gulsah; Ozdem, BernaGum Arabic (GA) is a clinically safe plant-derived polysaccharide with potential anti-cancer activity. We evaluated the effects of GA alone and in combination with ATG5 siRNA-mediated inhibition of autophagy in chemoresistant A2780-ADR ovarian cancer cells. GA at a concentration of 30.68 mu M reduced cell viability to 47 +/- 3% at 72 h and increased intracellular ROS 2.3-fold (n = 3, p < 0.001). The GA + ATG5 siRNA combination further decreased viability to similar to 30% and markedly enhanced apoptosis (Annexin V/PI, p < 0.001). Western blot analysis revealed increased p53 protein levels and decreased Bcl-2 protein levels, as well as altered P-Chk1 protein levels, which are consistent with apoptosis associated with DNA damage. GA also caused a loss of mitochondrial membrane potential and treatment-dependent changes in UCP4/5 expression, indicating mitochondrial stress. These findings identify GA, particularly in combination with autophagy inhibition, as a low-toxicity agent with significant anti-proliferative effects in vitro. The study is limited to cell models; in-vivo validation and pharmacokinetic/delivery studies are required before clinical translation. [GRAPHICS]Öğe Metformin induces mitochondria-mediated and endoplasmic reticulum stress-mediated apoptosis and inhibits angiogenesis-related gene expression in breast cancer cells via targeting VEGF-A/VEGFR2/NRP1(Medicinska Naklada, 2025) Alizade, Ares; Evyapan, Gulsah; Celik, Ibrahim Seyfettin; Ozdem, BernaAim To investigate the apoptotic and anti-angiogenic effects of metformin in human MCF7 breast cancer cells. Methods The effect of metformin on cell viability was assessed by MTS and crystal violet assays, and its effect on cell migration was evaluated by the wound healing assay. The gene expression and protein levels of angiogenesisand apoptosis-related genes were determined by realtime polymerase chain reaction, Western blot, and flow cytometry. Results Metformin reduced the viability and migration of breast cancer cells compared with the control group. Furthermore, metformin (10 mu M) increased the apoptosis-related gene and protein expression of caspase-3, Bax, AIF, CHOP and GRP78 48 hours after treatment compared with the control group. In contrast, it significantly decreased Bcl-2 and Wee1 gene and protein expression and suppressed angiogenesis-related genes VEGFA, VEGFR2, and NRP1. Conclusions Our results suggest that metformin treatment activates apoptosis pathways and inactivates the angiogenesis pathway. Although this study was conducted in vitro and did not directly evaluate blood vessel formation, the observed downregulation of angiogenesis-related genes suggests potential anti-angiogenic activity of metformin at the gene expression level.Öğe miRNAs in Melanoma: Diagnostic, prognostic, and therapeutic strategies(Biomedpress, 2024) Evyapan, Gulsah; Ozdem, Berna; Aksoy, GulsevincMelanoma is a highly aggressive and deadly form of skin cancer, with its incidence and mortality rates increasing significantly worldwide. Recent research suggests that miRNA-based therapies could help improve outcomes for melanoma patients by controlling gene expression at the post transcriptional level, which affects how the tumor grows and spreads. This review aims to examine the role of microRNAs (miRNAs) in melanoma progression, highlighting their potential as therapeutic targets and exploring how they may be utilized in diagnostic and prognostic processes.
