Catalpol promotes cellular apoptosis in human HCT116 colorectal cancer cells via microRNA-200 and the downregulation of PI3K-Akt signaling pathway.

Catalpol is an effective active ingredient that functions as a diuretic and laxative, and exhibits blood sugar-lowering, liver protective, anti-aging and anticancer effects. In traditional Chinese medicine, catalpol is believed to be Yin nourishing. The anticancer effect of catalpol on human HCT116 colorectal cancer cells were investigated and the mechanism of action was evaluated. Cellular viability was detected using an MTT assay. Caspase-3 and caspase-9 activity, cellular apoptosis and nucleic morphology were analyzed using caspase-3 and caspase-9 activity assay kits, flow cytometric assays and DAPI staining assay, respectively. Western blot analysis was used to measure the protein expressions of phosphatidylinositol 3-kinase (PI3K), phosphorylated-protein kinase B (p-Akt) and Akt. Expression of microRNA-200 was detected using the reverse transcription-quantitative polymerase chain reaction. HCT116 cells were incubated with PI3K inhibitors in order to analyze the effect of catalpol on cell proliferation. Catalpol was able to inhibit HCT116 cell proliferation. Furthermore, catalpol induced apoptosis in HCT116 cells, which depended on the increased activities of caspase-3 and -9. In addition, catalpol reduced the expression of PI3K, p-Akt and Akt in HCT116 cells. However, downregulation of PI3K/Akt decreased the viability of HCT116 cells following treatment with catalpol and enhanced microRNA-200 expression. Catalpol promoted cellular apoptosis in human HCT116 colorectal cancer cells through upregulation of microRNA-200 expression, which depended on a downregulation of the phosphatase and tensin homolog/PI3K-Akt signaling pathway.