Analysis of SIPA1 and RRP1B Gene Variants and Their Association with the Course of Cervical Cancer

Abstract

Background and Objectives The signal induced proliferation associated gene 1 (SIPA1) is a gene that modifies the onset of metastases, that activates GTPases (proteins that catalyze the hydrolysis of guanosine triphosphate), is involved in mitogen-induced cell cycle regulation, may enhance or stop cell cycle progression and plays an important role in regulating cell adhesion. Ribosomal RNA processing 1 homolog B (Rrp1b) interacts with SIPA1 and thus contributes to the regulation of the metastatic process. According to the literature, relationships between single nucleotide polymorphisms (SNPs) of these genes and tumor spread to regional lymph nodes in other oncological diseases have been identified, but their significance for cervical cancer as one of the most common oncological diseases progression is still poorly understood. We performed a study to investigate the distribution of SIPA1 gene functional polymorphisms (rs746429, rs931127) and RRP1B gene polymorphism (rs9306160) in a group of patients with cervical cancer. Then we analyzed the correlations between genotypes and alleles with tumor pathomorphological parameters and course of the disease. Material and Method 172 patients with cervical cancer were enrolled in the retrospective study. Subjects were recruited from October 2014 to August 2020. Clinical data on patients and peritheral blood sample were collected. Genomic DNA was extracted from leucocytes. Molecular genetic studies were performed using the real time polymerase chain reaction method. The obtained SNPs were used in further statistical analysis in genotype and allelic models. The statistical analysis was performed using SPSS. The associations between the genotypes and alleles with tumor characteristics were assessed using Pearson’s Chi-square or Fisher’s Exact tests. Univariate and multivariate analysis to present odds ratios with 95% confidence intervals (CIs) and p-values were calculat[...].