© 1995 Oxford University Press
research-article |
Cell proliferation and advancement of hepatocarcinogenesis in the rat are associated with a decrease in connexin 32 expression
Chemotherapy Division, National Cancer Center Research Institute 5-1-1, Tsukiji Chuo-ku, Tokyo 104
1Second Department of Pathology 5-1-1, Tsukiji Chuo-ku, Tokyo 104
2Department of Pediatric Surgery 5-1-1, Tsukiji Chuo-ku, Tokyo 104
3laboratory Animal Center, Fujita Health University School of Medicine Toyoakc, Aichi 470-11
4First Department of Pathology, Nagoya City University Medical School Nagoya 467, Japan
5International Agency for Research on Cancer Lyon Cedex 08, France
6To whom correspondence should be addressed
The expression of connexin 32 (Cx32), a major liver gap junction protein, after partial hepatectomy (PH) and during development and progression of hepatocarcinogenesis was studlled in the rat. Cx32 was quantitatively analyzed by counting iminunohistochemically demonstrated protein spots on the membranes of hepatocytes. Livers were sequen tially examined after PH to assess the correlation with cell proliferation. For the analysis of different stages in carcinogenesis, Cx32 was assayed in N-ethyl-N-hydroxy ethylnitrosamine-Induced enzyme altered foci (EAF), hyperplastic nodules (HN), hepatocellular carcinomas (HCC), pulmonary metastatic HCC and transplanted HCC In relation to their degree of altered enzyme expression. Cx32 showed: (i) a rapid decrease after PH to its lowest levels during and 12 h after the S phase of cell proliferation when 5-bromo-2'-deoxyundlne (BrdU) labeling indices were examined; (ii) a progressive decrease from early preneoplasia EAF to RN and HCC, values for pulmonary metastatic and transplanted HCC being 0; (iii) clearly Inverse correlations with increased BrdU Index and degree of altered enzyme expression in RN, indicating that these, with the lowest Cx32 count, are closest to HCC. Therefore, the observed decrease appears linked to cell proliferation and progression of hepatocarcinogenesis, providing a reflection of cellular independence and growth advantage.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  F. Marongiu, S. Doratiotto, S. Montisci, P. Pani, and E. Laconi Liver Repopulation and Carcinogenesis: Two Sides of the Same Coin? Am. J. Pathol., April 1, 2008; 172(4): 857 - 864. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Chida and M. Taguchi Localization of Alkaline Phosphatase and Proteins Related to Intercellular Junctions in Rat Hepatoma Cell Line McA-RH 7777 J. Histochem. Cytochem., July 1, 2004; 52(7): 979 - 983. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Gupta, P. Rajvanshi, H. Malhi, S. Slehria, R. P. Sokhi, S. R. G. Vasa, M. Dabeva, D. A. Shafritz, and A. Kerr Cell transplantation causes loss of gap junctions and activates GGT expression permanently in host liver Am J Physiol Gastrointest Liver Physiol, October 1, 2000; 279(4): G815 - G826. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. S. Isenberg, L. M. Kamendulis, J. H. Smith, D. C. Ackley, G. Pugh Jr., A. W. Lington, and J. E. Klaunig Effects of Di-2-Ethylhexyl Phthalate (DEHP) on Gap-Junctional Intercellular Communication (GJIC), DNA Synthesis, and Peroxisomal Beta Oxidation (PBOX) in Rat, Mouse, and Hamster Liver Toxicol. Sci., July 1, 2000; 56(1): 73 - 85. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. J. Elcock, E. Deag, R. A. Roberts, and J. K. Chipman Nafenopin Causes Protein Kinase C-Mediated Serine Phosphorylation and Loss of Function of Connexin 32 Protein in Rat Hepatocytes without Aberrant Expression or Localization Toxicol. Sci., July 1, 2000; 56(1): 86 - 94. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Green, A. Shilkaitis, and K. Christov 4-(Hydroxyphenyl)retinamide selectively inhibits the development and progression of ductal hyperplastic lesions and carcinoma in situ in mammary gland Carcinogenesis, August 1, 1999; 20(8): 1535 - 1540. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Bednarek, A. Shilkaitis, A. Green, R. Lubet, G. Kelloff, K. Christov, and C. M. Aldaz Suppression of cell proliferation and telomerase activity in 4-(hydroxyphenyl)retinamide-treated mammary tumors Carcinogenesis, May 1, 1999; 20(5): 879 - 883. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Ito, M. Tsuda, A. Yoshitake, T. Yanai, and T. Masegi Effect of Phenobarbital on Hepatic Gap Junctional Intercellular Communication in Rats Toxicol Pathol, March 1, 1998; 26(2): 253 - 259. [Abstract] [PDF]
|
|