Catalpol suppresses proliferation and facilitates apoptosis of MCF-7 breast cancer cells through upregulating microRNA-146a and downregulating matrix metalloproteinase-16 expression.

Breast cancer is the most common malignancy in women, and was the second highest cause of mortality in women in 2013. Matrix metalloproteinase-16 (MMP-16) is an enhancer of the invasion of breast cancer cells. The expression of microRNA‑146a (miR‑146a) has been reported to be significantly greater in patients with breast cancer compared with healthy controls. Catalpol is one of the main active ingredients of Rehmannia, of which the key pharmacological effects are antitumoral and antiproliferative. The present study was performed to investigate the effect of catalpol on breast cancer and to explore the potential therapeutic mechanisms. Cell proliferation was investigated using an MTT assay, and caspase‑3 activity assays and flow cytometry were used to assess apoptosis in MCF‑7 breast cancer cells. The expression levels of MMP‑16 and miR‑146a were investigated using gelatin zymography assays and reverse transcription-quantitative polymerase chain reaction, respectively. In addition, MCF‑7 cells were transfected with miR‑146a and anti‑miR‑146a to further investigate the effects of catalpol. The results demonstrated that catalpol reduced proliferation and promoted apoptosis in MCF‑7 cells, reducing MMP‑16 activity and increasing the expression of miR‑146a in MCF‑7 cells. This suggests that miR‑146a may regulate and control the expression levels of MMP‑16 in MCF‑7 cells. In conclusion, catalpol suppresses proliferation and facilitates apoptosis of MCF‑7 breast cancer cells through upregulating miR‑146a and downregulating MMP-16 expression.