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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 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, BernaBackgroundOvarian 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.Öğe Anatolian propolis extracts enhance cisplatin efficacy in ovarian cancer through AKT/mTOR pathway modulation and demonstrate antibacterial and antibiofilm activities(Humana Press Inc, 2025) Erdogan, Esra; Ozdem, Berna; Cimentepe, Ozge Ozturk; Tekedereli, IbrahimPropolis, a natural resinous substance rich in bioactive compounds, has been traditionally used for its therapeutic properties. This study investigates the cytotoxic and anticancer effects of Anatolian propolis on ovarian cancer cells, focusing on its modulation of the AKT/mTOR pathway and its ability to enhance cisplatin efficacy. Its antimicrobial and antibiofilm properties were also assessed, addressing infection risks in immunocompromised cancer patients. In epithelial ovarian cancer (A2780) cell line, apoptosis, cell cycle progression, and cell viability were evaluated using flow cytometric analysis, propidium iodide/annexin V staining, and MTS assay, respectively. The signaling pathways were analyzed using Western blotting. The IC50 value of propolis was determined as 0.342 +/- 0.180 mg/mL in the A2780 cell line and 1.11 +/- 0.31 mg/mL in the MCF-10A cell line. Apoptosis in the cells was evaluated using annexin V/PI staining and Caspase-3 expression via flow cytometry after treatment with varying concentrations of propolis and cisplatin. The combination of propolis at IC50 and cisplatin at IC25 demonstrated the highest apoptotic activity. Propolis treatment upregulated pro-apoptotic Bax while downregulating survival proteins (Bcl-2, mTOR/p-mTOR, and AKT/p-AKT) in A2780 cells, demonstrating AKT/mTOR pathway-mediated anticancer activity. Propolis exhibited potent antibacterial and antibiofilm activity against clinically relevant pathogens including MRSA and MDR E. coli, confirming its antimicrobial potential. Anatolian propolis demonstrates anticancer activity by modulating the AKT/mTOR pathway and enhancing cisplatin efficacy. Its antibacterial and antibiofilm properties further highlight its potential as a dual-function therapeutic agent, especially in cancer contexts where secondary infections are a common complication.Öğe 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]Öğe Cynarine Exhibits Antiproliferative Activity and Bcl-2-Mediated Apoptotic Cell Death in Breast Cancer Cells(Springer, 2024) Ozdem, Berna; Yildirim, Isil; Cetin, Ayten Kilincli; Tekedereli, IbrahimCynarine is a biologically active compound that is a derivative of hydroxycinnamic acid and can exhibit a structure-function relationship and therapeutic potential due to its bioactive properties. This study aimed to investigate the antiproliferative and apoptosis activity of the Cynarine compound in breast cancer cells in vitro. MDA-MB-231 MCF7 breast cancer cells and MCF 10A non-cancer cells were used. The MTT method was used to evaluate cell viability. Acolony-forming assay was employed on the cells treated with cynarine to assess their colony-forming capability. Western blotting and annexin-propidium iodide methods with flow cytometry were used to clarify its role in apoptosis. Cell proliferation and colony-forming abilities were reduced in cynarine-treated cells at 56.2%, 67, and 3% in MCF7 and MDA-MB 231, respectively. Apoptotic cell rates after 72 hours of cynarine treatment were found at 7.15%, 42.94%, and 68.67% in MCF 10A, MCF7, and MDA-MB-231 cell lines, respectively. Apoptosis was significantly different in MDA-MB-231 and MCF7 cells treated with cynarine (p < 0.05) It has been concluded that cynarine can be used as a combination therapeutic or a precursor compound to develop new drug combinations to treat breast cancer.Öğe Effect of humanine on the Notch signaling pathway in myocardial infarction(Tubitak Scientific & Technological Research Council Turkey, 2023) Onat, Elif; Onalan, Ebru; Ozdem, Berna; Balgetir, Merve Kavak; Kuloglu, TuncayBackground/aim: By applying humanin (HN) before myocardial infarction (MI), its protection in myocardial injury and the possible roles of its cellular mechanism in the Notch pathway were investigated. Materials and methods: The study was carried out at Firat University Experimental Research Center (12/24/2018-12/23/2019). Spraque-Dawley rats were divided into 10 groups: I (control) (n = 6), II (HN 6 h) (n = 6), III (HN 24 h) (n = 6), IV (HN day 7) (n = 6), V (MI 6 h) (n = 7), VI (MI 24 h) (n = 7), VII (MI day 7) (n = 7), VIII (MI+HN 6 h) (n = 7), IX (MI+HN 24 h) (n = 7), and X (MI+HN day 7) (n = 7). To create MI, 200 mg/kg of isoproterenol (ISO) was administered to the rats subcutaneously. Moreover, 252 mu g/kg of HN was given intraperitoneally (ip) to the rats on its own and before MI. Molecular parameters Notch1, Notch2, Hes1, Hes2, Jagged1, Jagged2, DLL1, and DLL4 were examined using polymerase chain reaction in the heart tissue, Notch1, Hes1, and DLL4 were examined using western blot, while heart tissue was taken for histochemical examinations. Results: The mRNA expression levels of the Notch signaling members (Notch1, Notch2, Hes1, Hes2, Jagged1, Jagged2, DLL1, and DLL4) tended to decrease after MI. The Notch signaling members increased more significantly, especially toward day 7 after HN application before MI. In the western blot anylyses, the Notch1, Hes1, and DLL4 protein levels increased significantly toward day 7 in the groups given HN before MI. Moreover, the serum AST, LDH, CK-MB, and troponin I levels tended to decrease with the application of HN before MI and there was a significant decrease in edema, hemorrhage, and mononuclear cells in the heart tissue at 24 h post-MI and fibrosis on day 7 post-MI. Conclusion: HN administration before MI has a cardioprotective effect on rats via the Notch signaling pathway.Öğe GRWD1 Drives Melanoma Growth Through NF-κB Signaling Pathway(Mattioli 1885, 2025) Turkmen, Dursun; Ozbey, Rafet; Ozdem, Berna; Alan, Saadet; Cetin, Ayten Kilincli; Baran, Fatma Bengisu; Dogan, BeratIntroduction: Melanoma is an aggressive skin cancer with high metastatic potential. The oncogenic protein GRWD1 has been implicated in various cancer types, but its role in melanoma remains unclear. Objectives: To examine the effects of GRWD1 knockdown on melanoma cell proliferation, apoptosis, and migration and to evaluate its prognostic significance in melanoma patients. Methods: A combination of in vitro and clinical analyses was performed. A2058 melanoma cells were treated with GRWD1-specific siRNA, and cell proliferation, apoptosis, and migration assays were conducted. Western blotting was used to assess alterations in key oncogenic pathways. Additionally, clinical tissue samples from melanoma patients were analyzed for GRWD1 expression, and Kaplan-Meier survival analysis was performed to determine its prognostic value. Results: GRWD1 was highly expressed in melanoma cells. GRWD1 knockdown significantly reduced cell proliferation (by 63%), impaired colony formation, and induced apoptosis (cleaved caspase-3 levels increased by 17.3%). Migration capacity decreased by 70%, and NF-kappa B pathway activity was suppressed, leading to reduced expression of Bcl-2, Src, and MDM2, while stabilizing p53. TCGA-based analyses revealed that high GRWD1 expression was significantly associated with shorter survival in metastatic melanoma cases (P=0.00029) but showed no correlation with melanoma subtypes. However, in immunohistochemical analysis of clinical samples, no statistically significant correlation was found between GRWD1 staining intensity and survival. Conclusions: GRWD1 plays a crucial role in melanoma progression by enhancing NF-kappa B activity, promoting proliferation, and suppressing apoptosis. While high GRWD1 expression is associated with poor prognosis in public datasets, further clinical validation with larger patient cohorts is needed to confirm its utility as a prognostic biomarker and therapeutic target.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.
