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Permanent URI for this collectionhttps://hdl.handle.net/11443/932

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Subject: search.filters.subject.LGALS3

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    Six potential biomarkers for bladder cancer: key proteins in cell-cycle division and apoptosis pathways
    (SPRINGER, 2022-01-01) Gultekin, Guldal Inal; Kahraman, Ozlem Timirci; Isbilen, Murat; Durmus, Saliha; Cakir, Tunahan; Yaylim, Ilhan; Isbir, Turgay
    Background: The bladder cancer (BC) pathology is caused by both exogenous environmental and endogenous molecular factors. Several genes have been implicated, but the molecular pathogenesis of BC and its subtypes remains debatable. The bioinformatic analysis evaluates high numbers of proteins in a single study, increasing the opportunity to identify possible biomarkers for disorders. Methods: The aim of this study is to identify biomarkers for the identification of BC using several bioinformatic analytical tools and methods. BC and normal samples were compared for each probeset with T test in GSE13507 and GSE37817 datasets, and statistical probesets were verified with GSE52519 and E-MTAB-1940 datasets. Differential gene expression, hierarchical clustering, gene ontology enrichment analysis, and heuristic online phenotype prediction algorithm methods were utilized. Statistically significant proteins were assessed in the Human Protein Atlas database. GSE13507 (6271 probesets) and GSE37817 (3267 probesets) data were significant after the extraction of probesets without gene annotation information. Common probesets in both datasets (2888) were further narrowed by analyzing the first 100 upregulated and downregulated probesets in BC samples. Results: Among the total 400 probesets, 68 were significant for both datasets with similar fold-change values (Pearson r: 0.995). Protein-protein interaction networks demonstrated strong interactions between CCNB1, BUB1B, and AURKB. The HPA database revealed similar protein expression levels for CKAP2L, AURKB, APIP, and LGALS3 both for BC and control samples. Conclusion: This study disclosed six candidate biomarkers for the early diagnosis of BC. It is suggested that these candidate proteins be investigated in a wet lab to identify their functions in BC pathology and possible treatment approaches.
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    LGALS3 and AXIN1 gene variants playing role in the Wnt/beta-catenin signaling pathway are associated with mucinous component and tumor size in colorectal cancer
    (ASSOC BASIC MEDICAL SCI FEDERATION BOSNIA \& HERZEGOVINA SARAJEVO, 2016-01-01) Korkmaz, Gurbet; Horozoglu, Cem; Arikan, Soykan; Gural, Zeynep; Saglam, Esra Kaytan; Turan, Saime; Ozkan, Nazli Ezgi; Kahraman, Ozlem Timirci; Yenilmez, Ezgi Nurdan; Duzkoylu, Yigit; Dogan, Mehmet Baki; Zeybek, Umit; Ergen, Arzu; Yaylim, Ilhan
    The Wnt pathway alterations have been identified in colorectal and many other cancer types. It has been reported that galectin-3 (which is encoded by the LGALS3 gene) alters the signaling mechanism in the Wnt/beta-catenin pathway by binding to beta-catenin in colon and other cancers. AXIN1 is mainly responsible for the assembly of the beta-catenin destruction complex in the Wnt pathway. This study investigated the relationship of rs4644 and rs4652 variants of the LGALS3 gene and rs214250 variants of the AXIN1 gene to histopathological and clinical properties. Our study included a total of 236 patients, of whom 119 had colorectal cancer (42 women, 77 men) and 117 were healthy controls. Polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) and allele-specific oligonucleotide (ASO) PCR methods were used. In addition, the serum galectin-3 level was studied with the enzyme-linked immunosorbent assay (ELISA) method. For the rs4644 variant of the LGALS(3) gene, the CC genotype a mucinous component was significantly more common than those without a mucinous component (p=0.026). C allele frequency of the rs214250 variant of the AXIN1 gene was significantly correlated to tumor size in the advanced tumor stage (p=0.022). The CCAACT haplotype was more common in colorectal cancer patients (p=0.022). Serum galectin-3 level was higher in the patient group compared to the control group (5.9 +/- 0.69 ng/ml vs. 0.79 +/- 0.01 ng/ml