Carcinogenesis · 1998 · 90 citations · 54 references
Life SciencesCell BiologyOncologyCarcinogenesisCell JunctionsNeoplasiaCancer Cell-cell CommunicationCell-cell JunctionsGap Junction CommunicationGap JunctionsIntercellular CommunicationAltered Intercellular CommunicationFluorescent Dye LabelingGap Junction Intercellular CommunicationGap Junctions In CancerNeoplastic DiseaseNeoplastic ProgressionTumor Suppressor Gene AlterationsTumor Suppressor Gene Loss
The reduced gap junctional intercellular communication (GJIC) and gap junction protein (connexin) expression that have been noted in many neoplastic cell types may contribute to the neoplastic phenotype. We assessed GJIC (by fluorescent dye micro-injection) and connexin expression (by Northern blotting, Western blotting and immunohistochemistry) in five mouse and 17 human lung carcinoma cell lines; both measures were lower in neoplastic cells compared to non-transformed lung epithelial cells. Other connexins were not detected in these cells. Co-culture experiments indicated that carcinoma cell lines able to transfer dye among themselves (homologous GJIC) had little capacity for dye-coupling with non-transformed cells (heterologous GJIC). Southern blot analyses indicated that reductions in GJIC and connexin43 expression were not due to deletions or rearrangements of this gene, but were more likely accounted for by transcriptional down-regulation and/or post-transcriptional factors. No correlations between GJIC and known oncogene and tumor suppressor gene alterations in the human lung carcinoma cells were apparent, suggesting that other mechanisms down-regulate GJIC in these cells. Since the neoplastic cell lines exhibited low GJIC (either homologous or heterologous), this characteristic may be involved in expression of the neoplastic phenotype.
54
E-cadherin-mediated cell-cell adhesion prevents invasiveness of human carcinoma cells.
U. Frixen, Jürgen Behrens, Matthew S. Sachs et al. · The Journal of Cell Biology · 1991 · 1.6K citations · Full text
Medicine, Cell Biology, Oncology +17