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Tight junction protein zo‐2 is differentially expressed in normal pancreatic ducts compared to human pancreatic adenocarcinoma
Author(s) -
Chlenski Alexandre,
Ketels Kathleen V.,
Tsao MingSound,
Talamonti Mark S.,
Anderson Marla R.,
Oyasu Ryoichi,
Scarpelli Dante G.
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19990702)82:1<137::aid-ijc23>3.0.co;2-f
Subject(s) - pancreatic duct , biology , pancreatic cancer , messenger rna , adenocarcinoma , microbiology and biotechnology , hamster , complementary dna , gene , peptide sequence , pancreas , endocrinology , cancer , biochemistry , genetics
Differential display of hamster mRNA identified a fragment present in normal pancreatic duct cells that is not expressed in pancreatic duct carcinoma cells. Sequence analysis showed an 88% and 82% identity, respectively, to the cDNA of the canine and human tight junction zo‐2 gene. Semi‐quantitative RT‐PCR analysis of human ZO‐2 revealed a striking difference in the expression of various regions of the ZO‐2 transcript in normal and neoplastic cells and the presence of an abnormality at the 5′‐end of mRNA. RACE analysis identified 2 human ZO‐2 mRNAs that encode proteins of different lengths, designated as ZO‐2A and ZO‐2C. The difference between the 2 forms of ZO‐2 is the absence of 23 amino acid residues at the N terminus of ZO‐2C compared with ZO‐2A. Although ZO‐2C was expressed in normal pancreatic cells and a majority of neoplastic tissues analyzed, ZO‐2A was undetectable except in one case in all of the pancreatic adenocarcinomas analyzed. This suggests the presence of a yet to be identified motif important for cell‐growth regulation within the 23–amino acid residue N‐terminal peptide of ZO‐2A, MPVRGDRGFPPRRELSGWLRAPG. Int. J. Cancer 82:137–144, 1999. © 1999 Wiley‐Liss, Inc.