Theasinensin a exerts anti-metastatic effects on HT-29 cells via downregulating the expression of MMP-9 and CCL2

Cancer metastasis, the terminal stage of cancer development, is accounting for approximately 90% of all human cancer mortalities. Previous research has suggested that theasinensin A (TSA) has anti-inflammatory effects; however, its potential for inhibiting colon cancer metastasis remains to be unclear. Therefore, in this research, we focused on investigating the mechanism of inhibitory effects of TSA on TPA-induced colon cancer cell migration. Previous studies show that matrix metalloproteinase-9 (MMP-9) and C-C motif ligand 2 (CCL2) are critical factors that cause cancer cell intravasation and extravasation. In our research, we tried to figure out if TSA can downregulate TPA-induced protein expression and activity of MMP-9 and CCL2 mRNA expression in human colon HT-29 cells. Our results showed that TSA effectively inhibited TPA-induced epithelial-mesenchymal transition (EMT), mesenchymal-epithelial transition (MET), cell anchorage-independent growth, and cell migration in HT-29 cells. Moreover, TSA may downregulate TPA-induced expression of MMP-9 and CCL2 via inhibiting TPA-induced phosphorylation of ERK.1/2 and p38 and AP-1 activation whereby further inhibit cancer cell migration. Our findings suggested that TSA could be a potential compound for preventing colon cancer metastasis.