The present study aimed to explore whether microcystin-LR (MC-LR; a well-known cyanobacterial toxin produced in eutrophic lakes or reservoirs) induced tumor progression by activating cadherin-11(CDH11). A previous tumor metastasis PCR array demonstrated that MC-LR exposure resulted in a significant increase in the expression of CDH11. In the present study, to confirm the effect of the MC-LR treatment on CDH11 expression, HT-29 cell migration and invasion following MC-LR treatment were tested by Transwell assays, and protein levels of CDH11 were tested by immunofluorescence and western blot analysis. The results demonstrated that MC-LR activated CDH11 expression in addition to cell migration and invasion in HT-29 cells. To further investigate the association between MC-LR-induced CDH11 upregulation, and higher motility and invasiveness in HT-29 cells, knockdown of CDH11 using small interfering RNA (siRNA) in HT-29 cells was performed. Subsequent Transwell assays confirmed that MC-LR-induced enhancement of migration and invasion was significantly decreased following CDH11 knockdown by CDH11-siRNA in HT-29 cells. The results from the present study indicate that MC-LR may act as a CDH11 activator to promote HT-29 cell migration and invasion.
Keywords: cadherin-11; colorectal cancer; invasion; microcystin-LR; migration.