Cell proliferation and advancement of hepatocarcinogenesis in the rat are associated with a decrease in connexin 32 expression

Hiroyuki Tsuda, Makoto Asamoto, Hiroyasu Baba, Yoshio Iwahori, Kazuyuki Matsumoto, Teruhiko Iwase, Yoshihisa Nishida, Shizuko Nagao, Katsuo Hakoi, Shuji Yamaguchi, Keisuke Ozaki, Hiroshi Yamasaki

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Abstract

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.

Original languageEnglish
Pages (from-to)101-105
Number of pages5
JournalCarcinogenesis
Volume16
Issue number1
DOIs
Publication statusPublished - 01-01-1995

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Hepatocellular Carcinoma
Cell Proliferation
Hepatectomy
Enzymes
Lung
Connexins
Liver
S Phase
connexin 32
Hepatocytes
Carcinogenesis
Membranes
Growth
Proteins

All Science Journal Classification (ASJC) codes

  • Cancer Research

Cite this

Tsuda, Hiroyuki ; Asamoto, Makoto ; Baba, Hiroyasu ; Iwahori, Yoshio ; Matsumoto, Kazuyuki ; Iwase, Teruhiko ; Nishida, Yoshihisa ; Nagao, Shizuko ; Hakoi, Katsuo ; Yamaguchi, Shuji ; Ozaki, Keisuke ; Yamasaki, Hiroshi. / Cell proliferation and advancement of hepatocarcinogenesis in the rat are associated with a decrease in connexin 32 expression. In: Carcinogenesis. 1995 ; Vol. 16, No. 1. pp. 101-105.
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abstract = "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.",
author = "Hiroyuki Tsuda and Makoto Asamoto and Hiroyasu Baba and Yoshio Iwahori and Kazuyuki Matsumoto and Teruhiko Iwase and Yoshihisa Nishida and Shizuko Nagao and Katsuo Hakoi and Shuji Yamaguchi and Keisuke Ozaki and Hiroshi Yamasaki",
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Tsuda, H, Asamoto, M, Baba, H, Iwahori, Y, Matsumoto, K, Iwase, T, Nishida, Y, Nagao, S, Hakoi, K, Yamaguchi, S, Ozaki, K & Yamasaki, H 1995, 'Cell proliferation and advancement of hepatocarcinogenesis in the rat are associated with a decrease in connexin 32 expression', Carcinogenesis, vol. 16, no. 1, pp. 101-105. https://doi.org/10.1093/carcin/16.1.101

Cell proliferation and advancement of hepatocarcinogenesis in the rat are associated with a decrease in connexin 32 expression. / Tsuda, Hiroyuki; Asamoto, Makoto; Baba, Hiroyasu; Iwahori, Yoshio; Matsumoto, Kazuyuki; Iwase, Teruhiko; Nishida, Yoshihisa; Nagao, Shizuko; Hakoi, Katsuo; Yamaguchi, Shuji; Ozaki, Keisuke; Yamasaki, Hiroshi.

In: Carcinogenesis, Vol. 16, No. 1, 01.01.1995, p. 101-105.

Research output: Contribution to journalArticle

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T1 - Cell proliferation and advancement of hepatocarcinogenesis in the rat are associated with a decrease in connexin 32 expression

AU - Tsuda, Hiroyuki

AU - Asamoto, Makoto

AU - Baba, Hiroyasu

AU - Iwahori, Yoshio

AU - Matsumoto, Kazuyuki

AU - Iwase, Teruhiko

AU - Nishida, Yoshihisa

AU - Nagao, Shizuko

AU - Hakoi, Katsuo

AU - Yamaguchi, Shuji

AU - Ozaki, Keisuke

AU - Yamasaki, Hiroshi

PY - 1995/1/1

Y1 - 1995/1/1

N2 - 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.

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