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The role of cadherin-11 in microcystin-LR-induced migration and invasion in colorectal carcinoma cells
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...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5774544/ https://www.ncbi.nlm.nih.gov/pubmed/29399188 http://dx.doi.org/10.3892/ol.2017.7458 |
Sumario: | 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. |
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