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Open Access Research article

Prostaglandin E2-EP1 and EP2 receptor signaling promotes apical junctional complex disassembly of Caco-2 human colorectal cancer cells

Marcelo N Tanaka1, Bruno L Diaz2, Wanderley de Souza3 and Jose A Morgado-Diaz1*

Author affiliations

1 Divisão de Biologia Celular, Coordenação de Pesquisa, Instituto Nacional de Câncer, Rua André Cavalcanti 37, 5° Andar, Rio de Janeiro, RJ, CEP: 20230-051, Brazil

2 Laboratório Intermediário de Inflamação, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Ilha do Fundão, 21941-902, Rio de Janeiro, RJ, Brazil

3 Laboratório de Ultraestrutura Celular Hertha Meyer, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Ilha do Fundão, 21941-902, Rio de Janeiro, RJ, Brazil

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Citation and License

BMC Cell Biology 2008, 9:63  doi:10.1186/1471-2121-9-63

Published: 2 December 2008



The apical junctional complex (AJC) is a dynamic structure responsible to maintain epithelial cell-cell adhesions and it plays important functions such as, polarity, mechanical integrity, and cell signaling. Alteration of this complex during pathological events leads to an impaired epithelial barrier by perturbation of the cell-cell adhesion system. Although clinical and experimental data indicate that prostaglandin E2 (PGE2) plays a critical function in promoting cell motility and cancer progression, little is known concerning its role in AJC disassembly, an event that takes place at the beginning of colorectal tumorigenesis. Using Caco-2 cells, a cell line derived from human colorectal cancer, we investigated the effects of prostaglandin E2 (PGE2) treatment on AJC assembly and function.


Exposition of Caco-2 cells to PGE2 promoted differential alteration of AJC protein distribution, as evidenced by immunofluorescence and immunoblotting analysis and impairs the barrier function, as seen by a decrease in the transepithelial electric resistance and an increase in the permeability to ruthenium red marker. We demonstrated the involvement of EP1 and EP2 prostaglandin E2 receptor subtypes in the modulation of the AJC disassembly caused by prostanoid. Furthermore, pharmacological inhibition of protein kinase-C, but not PKA and p38MAPK significantly prevented the PGE2 effects on the AJC disassembly.


Our findings strongly suggest a central role of Prostaglandin E2-EP1 and EP2 receptor signaling to mediate AJC disassembly through a mechanism that involves PKC and claudin-1 as important target for the TJ-related effects in human colorectal cancer cells (Caco-2).