Interference with the β-catenin gene in gastric cancer induces changes to the miRNA expression profile

Aberrant activation of the Wnt/beta-catenin signaling pathway plays a major role in carcinogenesis and the progression of many malignant tumors, especially gastric cancer (GC). Some research has suggested that expression of the beta-catenin protein is associated with clinicopathologic factors and affects the biological behaviors of GC cells. However, the mechanism of these effects is not yet clear. Studies show that the Wnt/beta-catenin pathway regulates some miRNAs. We hypothesize that oncogenic activation of beta-catenin signaling is involved in the formation of GC through regulating certain microRNAs (miRNAs). The results of the current study demonstrate that expression of the beta-catenin protein is associated with many clinicopathologic characteristics including the degree of differentiation, depth of tumor invasion, tumor site, and 5-year survival rate. We found that silencing the expression of beta-catenin with lentiviruses could delay cell proliferation, promote apoptosis, weaken the invasive power of GC cells, and increase the sensitivity of GC cells to 5-fluorouracil in vitro. Using miRNA microarrays to detect changes in the miRNA transcriptome following interference with beta-catenin in GC cells, we found that miR-1234-3p, miR-135b-5p, miR-210, and miR-4739 were commonly upregulated and that miR-20a-3p, miR-23b-5p, miR-335-3p, miR-423-5p, and miR-455-3p were commonly downregulated. These data provide a theoretical basis for the potential interaction between miRNA and the beta-catenin signaling pathway in GC.