P2.03-51 Gene Variants and Expressions of Galectin-3 Is Associated with Non Small Cell Lung Cancer and Vascular Invasion of the Tumor

Abstract

Galectin-3 is a β-galactoside binding protein and known for its deregulation in cancer. In previous studies, correlations between single nucleotide polymorphisms (SNP) and cancer development have been identified in the context of genetic susceptibility to different types of cancer. However, potential phenotypic variations related to galectin-3 SNPs have not yet been evaluated in non-small cell lung cancer (NSCLC). In this study, it was aimed to correlate expression levels of gene and protein galectin-3 with genotype and allele distribution of rs4644 and rs4652 SNPs of galectin-3 between NSCLC patients (n=65) and healthy control (n=95) individuals. SNPsrs4644 and rs4652 in galectin-3 were studied using TaqMan Real-Time PCR system. Tissue gene expression levels of galectin-3 for patients was also analysed by Real-Time PCR. Galektin-3 serum levels were measured by ELISA. There were no significant differences in genotype and allele distribution of SNPs and galectin-3 gene expression levels between the tumor tissues compared to tumor surrounding tissues (p> 0.05); Mean serum level of galectin-3 was significantly higher in patients (26.05 ± 1.77 ng / ml) than that of controls (11.62 ± 1.30 ng/ml) (p <0.0001). The presence of angiolymphatic invasion was statistically significantly associated with AA genotype (p = 0.04). SNP rs4644 AC/CC genotype was found to be associated with higher serum galectin-3 levels in patients compared to that of controls (p<0.0001) while SNP rs4652 with AA / AC genotype was associated with lower serum galectin-3 levels in controls compared to patients (p<0.0001). Serum galectin-3 level has been shown to be statistically significantly associated with of vascular invasion among patients who had AC genotypes for both SNPs rs4644 and rs4652 (p = 0.03; p = 0.019 respectively). Galectin-3 could be defined as a possible biomarker for NSCLC and it plays a role as surrogate marker for vascular invasion in tumors.