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Intercellular Communication in Bronchial Epithelial Cells: Review of Evidence for a Possible Role in Lung CarcinogenesisDepartment of Pathology, School of Medicine, University of Maryland, 22 South Greene Street, Baltimore, Maryland 21201 Department of Pathology, F. Edward Hebert School of Medicine, USUHS, Bethesda, Maryland
Department of Pathology, School of Medicine, University of Maryland, 22 South Greene Street, Baltimore, Maryland 21201 Department of Pathology, F. Edward Hebert School of Medicine, USUHS, Bethesda, Maryland
Department of Pathology, School of Medicine, University of Maryland, 22 South Greene Street, Baltimore, Maryland 21201 Department of Pathology, F. Edward Hebert School of Medicine, USUHS, Bethesda, Maryland
Department of Pathology, School of Medicine, University of Maryland, 22 South Greene Street, Baltimore, Maryland 21201 Department of Pathology, F. Edward Hebert School of Medicine, USUHS, Bethesda, Maryland
A challenging aspect of lung carcinogenesis is the elucidation of the mechanisms which permit initiated bronchial epithelial cells to attain a growth advantage over normal bronchial epithelial cells, and subsequently evolve into a malignant phenotype. In this review, the effects of interactions between normal and transformed cells, and the potential role of representative extrinsic factors on cell-cell communication are discussed. Evidence is presented to show how cell injury and the effects of serum and calcium may affect morphology and communication, and tumor development. A large number of autocrine-paracrine factors (e.g., TGFβ, TGF
Key Words: Bronchus • cancer • differentiation • gap junctions • growth factors • metabolic cooperation
Toxicologic Pathology, Vol. 18, No. 2,
324-343 (1990) |
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) are released by bronchial epithelial cells. These factors may inhibit or promote the proliferation of normal and transformed bronchial epithelial cells, respectively. The ability of certain injurious and tumor promoting agents (e.g., formaldehyde, TPA) to select for the transformed phenotype may involve selective cell injury, the induction of terminal differentiation and an inhibition of gap junction communication among normal BE cells.