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© 1994 Oxford University Press

research-article

Non-communicating human and murine carcinoma cells produce {alpha}1 gap junction mRNA

M. Mesnil 1, D. Rideout, N.M. Kumar and N.B. Gilula

Departments of Molecular Biology and Cell Biology, The Scripps Research Institute 10666 North Torrey Pines Road, La Jolla, CA 92037, USA

1To whom correspondence should be addressed at present address: Unit of Multistage Carcinogenesis, International Agency for Research on Cancer, 150 cours Albert Thomas, 69372 Lyon cedex 08, France

The gap junctional communication capacity of six human carcinoma-derived tumorigenic cell lines (pancreatic, pharyngeal and cervical), two murine carcinoma-derived tumorigenic cell lines (bladder-derived and Ehrlich ascites) and one monkey non-tumorigenic cell line (kidney epithelium) have been compared by the dye-transfer technique. All the tumorigenic cell lines were communication defective, while the non-tumorigenic cell line was not Moreover, six of the eight tumorigenic cell lines expressed a gap junction transcript coding for the connexin 43 ({alpha}1). Finally, gap junction plaques were not detected between tumorigenic cells by immunofluorescence staining. Consequently, these data suggest that communication defects in tumorigenic cells may result from either abnormally low levels of translation of junction mRNA or alterations in the assembly of junction protein into cell surface plaques, and not from failure to produce junction transcripts. Furthermore, since induction of {alpha}1 expression has been associated with dedifferentiation processes, the presence of {alpha}1 mRNA might be a characteristic property of certain tumorigenic cells that originate from cells that do not normally express {alpha}1 mRNA.


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