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Article

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

Carcinogenesis - 1 Jan 1995

Tsuda H, Asamoto M, Baba H, Iwahori Y, Matsumoto K, Iwase T, Nishida Y, Nagao S, Hakoi K, Yamaguchi S

Abstract excerpt

The expression of connexin 32 (Cx32), a major liver gap junction protein, after partial hepatectomy (PH) and during development and progression of hepatocarcinogenesis was studied in the rat. Cx32 was quantitatively analyzed by counting immunohistochemically demonstrated protein spots on the membranes of hepatocytes. Livers were sequentially examined after PH to assess the correlation with cell proliferation. For...

Topics

Animals
Bromodeoxyuridine
Cell Division
Connexins
Disease Progression
Hepatectomy
Immunohistochemistry
Liver
Liver Neoplasms, Experimental
Male
Phenotype

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Rats

Rats, Wistar

Gap Junction beta-1 Protein

Source

Identifiers

PMID: 7834792
DOI: 10.1093/carcin/16.1.101

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-7834792-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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Cell proliferation and advancement of hepatocarcinogenesis in the rat are associated with a decrease in connexin 32 expression.PMID 7834792Read ↗

WY-14,643-mediated promotion of hepatocarcinogenesis in connexin32-wild-type and connexin32-null mice.Semantic proximity Read ↗

Both early and late stages of hepatocarcinogenesis are enhanced in Cx32 dominant negative mutant transgenic rats with disrupted gap junctional intercellular communication.Semantic proximity Read ↗

The effect of connexin32 null mutation on hepatocarcinogenesis in different mouse strains.Semantic proximity Read ↗

Delayed liver regeneration and increased susceptibility to chemical hepatocarcinogenesis in transgenic mice expressing a dominant-negative mutant of connexin32 only in the liver.Semantic proximity Read ↗

Decreased connexin32 and a characteristic enzyme phenotype in clofibrate-induced preneoplastic lesions not shared with spontaneously occurring lesions in the rat liver.Semantic proximity Read ↗

Transgenic disruption of gap junctional intercellular communication enhances early but not late stage hepatocarcinogenesis in the rat.Semantic proximity Read ↗

Role of connexin32 and beta-catenin in tumor promotion in mouse liver.Semantic proximity Read ↗

Altered homologous and heterologous gap-junctional intercellular communication in primary human liver tumors associated with aberrant protein localization but not gene mutation of connexin 32.Semantic proximity Read ↗

Involvement of gap junctions in tumor suppression: analysis of genetically-manipulated mice.Semantic proximity Read ↗

Background lesions during a 24-month observation period in connexin 32-deficient mice.Semantic proximity Read ↗

Reduction of malignant phenotype of HEPG2 cell is associated with the expression of connexin 26 but not connexin 32.Semantic proximity Read ↗

Neoplastic phenotype of gap-junctional intercellular communication-deficient WB rat liver epithelial cells and its reversal by forced expression of connexin 32.Semantic proximity Read ↗

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