Identification of relationships among EDIL3, angiogenesis and inflammation in colorectal cancer: In-silico analysis

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dc.authoridIlikci Sagkan, Rahsan/0000-0003-3844-6158
dc.contributor.authorSagkan, Rahsan Ilikci
dc.contributor.authorBali, Dilara Fatma Akin
dc.date.accessioned2024-11-07T13:32:07Z
dc.date.available2024-11-07T13:32:07Z
dc.date.issued2021
dc.departmentNiğde Ömer Halisdemir Üniversitesi
dc.description.abstractAim: 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.
dc.identifier.doi10.4328/ACAM.20268
dc.identifier.endpage280
dc.identifier.issn2667-663X
dc.identifier.issue3
dc.identifier.startpage274
dc.identifier.urihttps://doi.org/10.4328/ACAM.20268
dc.identifier.urihttps://hdl.handle.net/11480/15241
dc.identifier.volume12
dc.identifier.wosWOS:000645102100010
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.language.isoen
dc.publisherBayrakol Medical Publisher
dc.relation.ispartofAnnals of Clinical and Analytical Medicine
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_20241106
dc.subjectEDIL3/DEL-1
dc.subjectColon cancer
dc.subjectInflammation
dc.subjectMutation
dc.subjectGene expression
dc.subjectAngiogenesis
dc.titleIdentification of relationships among EDIL3, angiogenesis and inflammation in colorectal cancer: In-silico analysis
dc.typeArticle

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