Background
miR-30a is a microRNA associated with the progression of malignant tumors such as gastric cancer, colon cancer, prostate cancer, and lung cancer, and can regulate the proliferation and migration of breast cancer (BC) cells in vitro. However, its expression, function, clinical significance and relationship with the Wnt/β-catenin pathway in human BC were still unclear.
Conclusion
miR-30a was lowly expressed in breast cancer tissues and highly in β-catenin protein, and miR-30a might block the Wnt/β-catenin pathway by inhibiting the accumulation of β-catenin, and then inhibiting breast cancer progression.
Methods
Immunohistochemistry, Western blotting and real-time quantitative PCR (RT-qPCR) were used to measure the expressions of miR-30a and β-catenin in 114 pairs of human BC tumor tissues and adjacent normal tissues which were collected from March 2014 to October 2015. The effect of miR-30a on the expression of β-catenin was studied in the MCF-7 cells in vitro.
Results
The expression levels of miR-30a in human BC tumor tissues were significantly lower than they were in the adjacent normal tissues (P < 0.001), and significantly higher in β-catenin protein (P < 0.001), but there was no significant different in β-catenin mRNA (P = 0.3816). The immunohistochemistry results showed that β-catenin protein was only expressed on the cell membrane in paracancerous normal tissues, but β-catenin protein was expressed on the cell membrane and cytoplasm in BC tumor cells. In addition, there was a significantly negative correlation (r = -0.816, P < 0.001) between the expression miR-30a and β-catenin protein in BC tissues. The age of onset, PR expression, ER expression, and HER-2 expression of the BC patients were not related to miR-30a or β-catenin protein expression (P > 0.05). Tumor diameter, histological grade, lymph node metastasis, TNM stage, and the prognosis of BC patients (P < 0.05) were significantly related to miR-30a or β-catenin protein expression. In MCF-7 cells, miR-30a regulated the accumulation of β-catenin protein by inhibiting the expression of BCL9 in BC cells.