Anillin is a prognostic factor and is correlated with genovariation in pancreatic cancer based on databases analysis.

Pancreatic cancer has a low survival rate globally. Anillin (ANLN) is involved in the pathogenesis of pancreatic cancer (PC). The present study used databases and reverse transcription-quantitative PCR to investigate the association between ANLN expression, clinical variables and the survival rate of patients with pancreatic cancer. Gene expression of ANLN in normal and cancer tissues was analyzed using data from The Cancer Genome Atlas, Oncomine and Gene Expression database of Normal and Tumor tissues 2 and ANOVA, and the association between ANLN mRNA expression and ANLN genovariation was analyzed using cBioPortal. The association between ANLN expression and the survival, clinical, pathological and prognostic characteristics of PC was analyzed using Kaplan-Meier (K-M) survival analysis, Kruskal Wallis and Mann Whitney-U tests, and logistic and Cox regression models. Gene Set Enrichment Analysis (GSEA) revealed the molecular pathways underpinning ANLN function in PC. Overexpression of ANLN was observed in PC cells (normal vs. tumor, P<0.01) and tissues (normal vs. tumor, P=0.008). Enhanced ANLN expression was associated with high tumor grade (grade 1 vs. grade 3, odds ratio: 5.662, P<0.001). However, ANLN expression was not associated with other clinical features (all P>0.05). K-M analysis suggested that increased ANLN expression was associated with poor survival (P=0.002). Univariate and multivariate analysis revealed the ANLN is an independent prognostic factor for PC (P<0.001). GSEA demonstrated the p53, cell cycle, DNA replication, mismatch repair, nucleotide excision repair and PC pathways were associated with low expression of ANLN. Overall, ANLN is more highly expressed in PC compared with in normal tissue, and is associated with poor differentiation. The expression of ANLN may be a novel prognostic marker of poor survival. Finally, ANLN exert its functions in PC through the p53, cell cycle, DNA replication, mismatch repair and nucleotide excision repair and pathways.