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    Anticancer activity of sinapic acid by inducing apoptosis in HT-29 human colon cancer cell line
    (Canadian Science Publishing, 2023) Tastemur, Seyma; Hacisuleyman, Levent; Karata, Ozhan; Yulak, Fatih; Ataseven, Hilmi
    Colorectal cancer is the third most lethal and fourth most commonly diagnosed cancer worldwide. Sinapic acid, a derivative of hydroxycinnamic acid, is a promising phytochemical exhibiting numerous pharmacological activities in various systems. It is a substantial chain-breaking antioxidant that operates as a radical scavenger. The aim of this research was to investigate the antiproliferative effect of sinapic acid on the HT-29 cell line besides the mechanisms underlying this activity. The effect of sinapic acid on the viability of HT-29 cell line was investigated using XTT assay. The levels of BCL-2, cleaved caspase 3, BAX, cleaved PARP, and 8-oxo-dG were measured using ELISA. Gamma-H2AX and cytochrome c expressions were assessed semiquantitatively using immunofluorescence staining. Sinapic acid at 200 & mu;m and higher doses produced a significant antiproliferative effect on HT-29 cells. The IC50 value was found to be 317.5 & mu;m for 24 h. Sinapic acid (317.5 & mu;m) significantly elevated cleaved caspase 3, BAX, cleaved PARP, and 8-oxo-dG levels. The levels of gamma-H2AX foci are significantly higher, while the levels of cytochrome c are lower in sinapic acid-treated HT-29 cells. These results indicate that sinapic acid has antiproliferative, apoptotic, and genotoxic effects on colon cancer cells.
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    Effects of dexpanthenol on 5-fluorouraci-induced nephrotoxicity, hepatotoxicity, and intestinal mucositis in rats: a clinical, biochemical, and pathological study
    (Walter De Gruyter Gmbh, 2025) Tastemur, Seyma; Ekici, Mehmet; Mendil, Ali Sefa; Ozkaraca, Mustafa; Ataseven, Hilmi
    Background5-fluorouracil (5-FU) is a broad-spectrum drug that has a wide range of side effects. Patients may experience severe comorbidities as a result of these toxic side effects, making it impossible for them to continue chemotherapy. Despite the fact that various molecules have been experimented, there is no literature data on the efficacy of dexpanthenol (DXP) for mitigating the toxic effects of 5-FU.ObjectiveTo investigate the protective effects of DXP on nephrotoxicity, hepatotoxicity, and intestinal toxicity induced by 5-FU in rats.MethodsTwenty-eight male Wistar-Albino rats aged 16 weeks were randomly assigned to four groups. We created a rat model of intestinal mucositis, nephrotoxicity, and hepatotoxicity through intraperitoneal 5-FU (35 mg/kg for 4 d) injection. 500 mg/kg and 1000 mg/kg of DXP were administered to the treatment groups. The effects of dexpanthenol were evaluated clinically, biochemically, histopathologically, and immunohistochemically (inducible nitric oxide synthase [iNOS], cyclooxygenase-2 [COX-2], 8-hydroxyguanosine [8-OHdG], and nuclear factor kappa B [NF-kappa B]).Results5-FU caused a decrease in body weight and food intake, and an increase in diarrhea scores in rats. 5-FU led to significant disruptions in the hepatic biochemical markers (aspartate transaminase [AST], alanine transaminase [ALT], alkaline phosphatase [ALP], total bilirubin, direct bilirubin, and lactate dehydrogenase [LDH]), renal biochemical markers (blood urea nitrogen [BUN], creatinine, and uric acid), and protein and albumin, which are markers of both hepatic and renal functions. Severe pyknosis and mononuclear cell infiltrations were observed in the liver, and mononuclear cell infiltration and tubular degeneration in the kidneys. Jejunum and colon showed villous hyperemia and hemorrhage, respectively, along with mononuclear cell infiltration. Furthermore, 5-FU increased the immunohistochemical expressions of iNOS, COX-2, 8-OHdG, and NF-kappa B in the examined tissues. The administration of DXP at doses of 500 mg/kg and 1000 mg/kg demonstrated significant mitigation of the toxic effects induced by 5-FU on the liver, kidney, jejunum, and colon.ConclusionDXP showed protective effects against nephrotoxicity, hepatotoxicity, and intestinal toxicity caused by 5-FU. These findings suggest that DXP may serve as a potential therapeutic agent to alleviate the severe side effects of 5-FU chemotherapy, thereby improving patient tolerance and quality of life. Further clinical studies are warranted to validate these results and explore the translational potential of DXP in human cancer therapy.
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    GSK461364A suppresses proliferation of gastric cancer cells and induces apoptosis
    (Pergamon-Elsevier Science Ltd, 2023) Ataseven, Dilara; Tastemur, Seyma; Yulak, Fatih; Karabulut, Sebahattin; Ergul, Mustafa
    Polo-like kinase 1 (PLK1) is crucial in regulating cell division and has been shown to have an oncogenic function in several cancers. Since PLK1 overexpression is closely related to tumorigenesis and has been correlated with poor clinical outcomes, specific inhibition of PLK1 in cancer cells is a promising approach for developing new anticancer drugs. In this context, the aim of the present study was to evaluated the potential cytotoxic effects of GSK461364A, a competitive inhibitor for PLK1, in gastric cancer cell line SNU-1 cells and explored its cytotoxic mechanism. The cells were exposed to GSK461364A at different concentrations ranging from 1 to 40 mu M for 24 h, and it showed considerable cytotoxicity with an IC50 value of 4.34 mu M. The treatment of SNU-1 cells with GSK461364A results in cell cycle arrest at the G2/M phase, decreased mitochondrial membrane potential, and increased apoptosis as indicated by Annexin V binding assay. In addition, GSK461364A treatment significantly increased the total oxidant (TOS) level, a signal of oxidative stress, and increased cleaved PARP and 8-oxo-dG levels as an indicator of DNA damage. ELISA experiments evaluating Bax, BCL-2, and cleaved caspase 3 also confirmed the apoptotic effect of GSK461364A. Current findings suggest that GSK461364A may be a chemotherapeutic agent in patients with gastric cancer. Nevertheless, more research is needed to evaluate GSK461364A as a cancer treatment drug.
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    In vitro comparison of the cytotoxic effects of lenalidomide alone and in combination with verapamil on myeloma cell line
    (Wolters Kluwer Medknow Publications, 2021) Tastemur, Seyma; Sencan, Mehmet; Terzi, Hatice; Ergul, Merve; Tastemur, Mercan
    Introduction Multiple myeloma (MM) is a malignant hematological disease characterized by monoclonal proliferation of plasma cells. High-dose chemotherapy with novel agents and autologous stem cell transplantation are options for treatment. However, MM treatment generally results in failure. The most important reason for this failure is the resistance to chemotherapeutic drugs. Various studies have been tried to combine chemosensitizer agents that increase the cytotoxic effects of the chemotherapeutics to eliminate the drug resistance. In our study, we aimed to evaluate the effect of verapamil on the cytotoxic effect of lenalidomide on the myeloma cell line. Materials and methods Verapamil is a chemosensitizer that suppresses the P-glycoprotein. In our study, lenalidomide, an immunomodulatory agent, was compared alone and in combination with verapamil for cytotoxic effects. U266 MM cell line was used in the study. At the concentrations of 0.001, 0.01, 0.1, 1, 10, 50, and 100 mu M, lenalidomide alone and the combination of lenalidomide at the same concentrations with 2.5 mu g/ml of verapamil were compared in terms of possible cytotoxic properties. Cell viability was measured by XTT (2,3-bis (2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino) carbonyl]-2H-tetrazolium hydroxide) test. Results A statistically significant decrease in the inhibitor concentration, causing 50% decrease in cell proliferation (IC50) of lenalidomide, was provided via verapamil administration. Our study revealed that the cytotoxic effect of lenalidomide increases when combined with verapamil. Conclusion We aimed to understand whether the cytotoxic effect of lenalidomide, which has an important place in the treatment of MM, can be increased with an easily available drug such as verapamil. We think that more studies and meta-analyses are needed owing to the different results related to the subject in the literature, and we hope to set an example for new studies. (C) 2021 The Egyptian Journal of Haematology
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    Is it possible to use Proton Pump Inhibitors in COVID-19 treatment and prophylaxis?
    (Elsevier, 2020) Tastemur, Seyma; Ataseven, Hilmi
    Coronaviruses (CoV), discovered after 1960, caused human life-threatening outbreaks. SARS-CoV2, which appeared in Wuhan, China in December 2019, causing Severe Acute Respiratory Syndrome and has different features than other coronaviruses, has been determined and the disease caused by the virus has been called Coronavirus Disease-2019 (COVID-19). This disease activates both the natural and acquired immune system. The cytokin storm, in which blood levels of proinflammatory cytokines are detected excessively high is developing and the uncontrolled inflammatory response causes local and systemic tissue damages. Although a spesific drug has not been found yet, the medications currently in use for other indications, whose pharmacokineticpharmacodynamic properties and toxic doses are already known; are included in the treatment practice of COVID-19. These drugs affect the entry of the virus into the cell and its intracellular distribution. They also have anti-inflammatory and immunomodulating effects too. Therefore, we think that Proton Pump Inhibitors (PPI's) with similar mechanisms of action may also be involved in COVID-19 treatment and prophylaxis.
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    Methylation profile of CD247 and FOXP3 genes and frequency of certain HLA-DQ haplotypes in Celiac disease
    (Elsevier Masson, Corp Off, 2025) Yildirim, Malik Ejder; Ataseven, Hilmi; Kurtulgan, Hande Kucuk; Tastemur, Seyma; Sirin, Ahmet
    Background: Celiac disease is an autoimmune disorder that affects the small intestine in people with gluten intolerance. HLA-DQ2 and DQ8 have been associated with Celiac Disease. CD247 is a subunit of the T cell receptor complex and Forkhead box P3 (FOXP3) is a transcription factor involved in the regulation of the immune response. Expression levels of these two markers in various diseases, including autoimmune disorders, are controversial. In this context, we aimed to shed light on the etiopathogenesis of Celiac disease by determining the methylation profile of CD247 and FOXP3 genes, and to calculate the frequency of HLA-DQ haplotypes in this disease. Methods: Methylated and unmethylated copy numbers of the CD247 and FOXP3 genes in samples were calculated using the methylation-specific qPCR method. The records regarding HLA-DQ2 and DQ8 genotypes previously detected from our patients by Real Time PCR and tissue transglutaminase IgA (TTG-IgA) by ELISA, were analyzed. Results: CD247 methylation rate in our patients was significantly lower than in controls. According to the Marsh classification, the methylation level in Marsh type 2-3 patients was statistically lower than in type 1. On the contrary, FOXP3 had a significantly higher methylation rate in the patient group compared to healthy controls, and this gene was also found to be more methylated in Marsh type 2-3 patients than in Marsh type 1. In the patient group, HLA-DQ2 positivity was 82.5% and HLA-DQ8 positivity was 37.5%. Conclusion: The data suggest that CD247 expression is upregulated, whereas FOXP3 expression is downregulated in Celiac disease. Among HLA haplotypes, HLA-DQ2 heterodimer came to the forefront with its frequency in terms of celiac predisposition.