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Regulation of tight junctions in human normal pancreatic duct epithelial cells and cancer cells
Author(s) -
Kojima Takashi,
Sawada Norimasa
Publication year - 2012
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2012.06579.x
Subject(s) - occludin , pancreatic cancer , transfection , telomerase reverse transcriptase , tight junction , cancer cell , microbiology and biotechnology , cancer research , chemistry , biology , cell culture , telomerase , cancer , medicine , gene , biochemistry , genetics
To investigate the regulation of tight junction molecules in normal human pancreatic duct epithelial (HPDE) cells and pancreatic cancer cells, we introduced the human telomerase reverse transcriptase (hTERT) gene into HPDE cells in primary culture and compared them to pancreatic cancer cell lines. The hTERT‐transfected HPDE cells were positive for PDE markers and expressed claudin‐1, claudin‐4, claudin‐7, and claudin‐18, occludin, tricellulin, marvelD3, JAM‐A, zonula occludens (ZO)‐1, and ZO‐2. The tight junction molecules, including claudin‐4 and claudin‐18 of normal HPDE cells, were in part regulated via a protein kinase C signal pathway by transcriptional control. In addition, claudin‐18 in normal HPDE cells and pancreatic cancer cells was markedly induced by a PKC activator, and claudin‐18 in pancreatic cancer cells was also modified by DNA methylation. In the marvel family of normal HPDE cells and pancreatic cancer cells, tricellulin was upregulated via a c‐Jun N‐terminal kinase pathway, and marvelD3 was downregulated during Snail‐induced epithelial–mesenchymal transition.