Upregulation of miR-222 in both Helicobacter pylori- infected and noninfected gastric cancer patients.

Despite of promising improvements in treatment of gastric cancer, the mortality rate of this malignancy remains high. Chronic infection by Helicobacter pylori, interfering with intracellular signalling pathways, is the main risk factor for gastric cancer. Some evidence suggests that microRNAs (miRNA), the small noncoding RNA molecules, can play role as oncogenes or tumour suppressors in the cells. MiR-222 is one of the remarkable miRNAs undergoing upregulation in gastric cancer. However, the association between miR-222 upregulation and H. pylori infection in gastric cancer tissues remains unclear. The aim of this study was to analyse the expression level of miR-222 in gastric cancer tissues, evaluating the relationship between miR-222 expression level and H. pylori infection and also finding novel miR-222 targets based on in silico investigations. MiR-222 expression level in 200 patients including 112 H. pylori positive and 88 H. pylori negative was relatively measured using RT-qPCR and compared with 88 healthy samples. In silico enrichment analysis of miR-222 targets was performed by DAVID database to evaluate the possible role(s) of miR-222 in gastric tumourigenesis. We observed upregulated level of miR-222 in gastric cancer tissues compared with normal samples (P<0.05). However, no significant difference between miR-222 expression in H. pylori-positive and H. pylori-negative cases was observed. Our in silico analyses showed the possible role of p53, p27, PTEN and Elongin B in gastric cancer tumourigenesis. MiR-222 functions as an onco-miRNA and its overexpression can be involved in pathogenesis of gastric cancer, independent of H. pylori infection.