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    Epidermal Growth Factor-Like Repeats and Discoidin I-Like Domains 3 is a Novel Regulator of Epithelial-Mesenchymal Transition in Clear Cell Renal Cell Carcinoma: In Silico Analysis
    (Erciyes Univ Sch Medicine, 2021) Sagkan, Rahsan Ilikci; Bali, Dilara Fatma Akin
    Objective: Epithelial-mesenchymal transition (EMT) contributes to cancer metastasis and recurrence, which are major obstacles in changing the course of cancer. However, studies on the mutational and gene expression profiles of epidermal growth factor-like repeats and discoidin I-like domains 3 (EDIL3) that reveal the relationship between clear cell renal cell carcinoma (ccRCC) and EMT markers are limited. The aim of our study was to reveal the correlation between tumor and EMT markers (E-cadherin and vimentin) and EDIL3 expression. Additionally, we evaluated target gene expression levels and mutational profiles in kidney cancer tissue and normal tissue. Materials and Methods: We investigated the mutational profile and mRNA expression of EDIL3 and compared them with that of VIM and CDH1 in 523 patients with ccRCC using validated bioinformatics analysis. Additionally, Polymorphism Phenotyping v2 (PolyPhen-2), Screening for NonAcceptable Polymorphisms (SNAP) were used to predict and confirm the pathogenicity of the mutations detected. Studies were performed in silico using bioinformatics tools. Results: EDIL3 and VIM expression was statistically significantly higher in the healthy group and exhibited a positive correlation in patients with ccRCC. Patients with elevated VIM and CDH1 expression and low EDIL3 expression had prolonged survival time. In addition, 7 mutations were detected in the evaluated genes, 6 of which had potential pathogenic features. Conclusion: Our study provides insights for further experimental studies. EDIL3 can be used as a diagnostic or prognostic indicator of cancer development to help cure renal clear cell cancer.
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    Genetic and epigenetic concept of SARS-CoV-2 targets in different renal cancer subtypes
    (Walter De Gruyter Gmbh, 2021) Akin-Bali, Dilara Fatma; Sagkan, Rahsan Ilikci
    Objectives: Recent advances in defining the genetic landscape of has shown the host cell-SARS-CoV-2 interaction via ACE2 protein and the presence of at least three additional virus invasion genes including TMPRSS2, FURIN, CD147/BSG. In current study, we investigated the mutation and m-RNA expression patterns of target genes by evaluating the associations between genetic and epigenetic mechanisms in the target genes and susceptibility of SARS-CoV-2 infection of renal cancer subtypes. Methods: We investigated the mutation and m-RNA expression patterns of our target genes. The promoter methylation profiles of target genes were tested in the UALCAN database. Results: The total rate of carrying genetic anomaly in the target genes including was 1.6% and seven mutations, one of which had a pathogenic feature, were detected. The expression analysis results in renal cancer groups showed that while the KIRC and KIRP patients had a lower level of TMPRSS2 than the healthy control, their ACE2 level was high. KICH patients had a higher level of CD147/BSG expression than the healthy group. The promoter methylation levels of ACE2 in KIRC and KIRP were reduced. Conclusions: We concluded that renal cancer patients may be more sensitive to SARS-CoV-2 infection, which may worsen the prognosis.
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    Identification of relationships among EDIL3, angiogenesis and inflammation in colorectal cancer: In-silico analysis
    (Bayrakol Medical Publisher, 2021) Sagkan, Rahsan Ilikci; Bali, Dilara Fatma Akin
    Aim: The relationship between inflammation and the development of colorectal adenocarcinoma has been described for a number of years. In this cancer, chronic inflammation causes cellular damage and DNA mutations responsible for the proliferation of transformed cells. Epidermal growth factor-like repeats and discoidin I-like domains 3 (EDIL3/DEL-1) were anti-inflammatory protein, especially in epithelial cells. Our study, it was aimed to clarify the link of among IL-17A, EDIL3/DEL1, and the main angiogenic factor VEGFA/B in colorectal cancer. Materials and Methods: We investigated EDIL3, IL-17, and VEFGA/B mutations profile and levels of m-RNA expressions in 594 colorectal cancer patients using bioinformatics analysis for the revealing relationship among these molecules. Additionally, PolyPhen-2 and SNAP tools were used to predict and confirm the pathogenicity of the detected mutations. Results: In colorectal cancer patients, the IL-17 and EDIL3 expressions were inversely correlated but the low correlation coefficient was statistically significant. EDIL3 and VEGFB m-RNA levels were found to be statistically significantly lower in the patient group than in the healthy group. Furthermore, 10 mutations were identified in the EDIL3. The study predicted the potential pathological effect of eight mutations in the EDIL3. Discussion: Low expression of EDIL3 might contribute to anti-inflammation, supporting extravasation of leukocytes to inflammatory area by increased IL-17 expression. Although further studies to clarify the mechanisms explaining the role of EDIL3 in tumor angiogenesis in terms of VEGF gene, and the interaction between IL-17 and EDIL3 are required, the results indicate that EDIL3 may be a good novel molecular target gene in inflammatory pathways for colorectal cancer.
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    Mutations and Expression Profile of EDIL3 and Correlation with HIF1A and Tumor-Associated Carbonic Anhydrases in Pancreatic Cancer
    (Marmara Univ, Inst Health Sciences, 2021) Bali, Dilara Fatma Akin; Sagkan, Rahsan Ilikci
    Objective: Epidermal growth factor-like repeats and discoidin I-like domains 3 (EDIL3) expression is upregulated in some types of cancer which means that it can be used as a candidate tumor marker. The expression level of EDIL3 as a marker of the hypoxic microenvironment of pancreatic cancer was assessed by studying its relationship with the expression of tumor-associated carbonic anhydrases (CA IX and CA XII) and Hypoxia-inducible factor-1 (HIF-1) in tumor development. Methods: Gene expression and mutation profiles of pancreatic cancer patients and healthy tissue samples were downloaded The Cancer Genome Atlas (TCGA), and the genetic alterations and expression levels of the EDIL3, HIF-1 alpha, CA IX and CA XII genes were analyzed. Additionally, PolyPhen-2 and SNAP tools were used to prediction and confirmation of detected alterations pathogenicity and survival analysis was performed. Results: Expression levels of EDIL3, HIF-1 alpha and CA IX were found to be statistically significant higher in the patient compared to healthy group and we showed also positive correlation between EDIL3 and HIF-1 alpha gene expression. Furthermore, low CA IX and CA XII expression levels were found effective on overall survival (p<0.05). Additionally, 8 missense mutations were detected in the coding region of studied genes. Conclusion: We suggested that relationship between EDIL3 and HIF-1 alpha in pancreatic cancer and EDIL3 is a novel molecule cancer development in pancreatic cancer.