INTERCELLULAR COMMUNICATION IN BRONCHIAL EPITHELIAL-CELLS - REVIEW OF EVIDENCE FOR A POSSIBLE ROLE IN LUNG CARCINOGENESIS

被引：13

作者：

ALBRIGHT, CD ^{[1
]}

JONES, RT ^{[1
]}

GRIMLEY, PM ^{[1
]}

RESAU, JH ^{[1
]}

机构：

[1] UNIV MARYLAND,SCH MED,DEPT PATHOL,22 S GREENE ST,BALTIMORE,MD 21201

来源：

TOXICOLOGIC PATHOLOGY | 1990年 / 18卷 / 02期

关键词：

Bronchus; Cancer; Differentiation; Gap junctions; Growth factors; Metabolic cooperation;

D O I：

10.1177/019262339001800211

中图分类号：

R36 [病理学];

学科分类号：

100104 ;

摘要：

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., TGFB, TGFα) 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. © 1990, SAGE Publications. All rights reserved.

引用

页码：324 / 341

页数：18

共 175 条

[51]

Gordon R.E., Lane B.R., Marin M, Regeneration of rat tracheal epithelium: Changes in gap junctions during specific phases of the cell cycle, Exp. Lung Res., 3, pp. 47-56, (1982)

[52]

Gorman R.R., Wieranga W, Miller O.V., Independence of the cyclic AMP-lowering activity of thromboxane A2 from the platelet release reaction, Biochem. Biophys. Acta, 572, pp. 95-104, (1979)

[53]

Grafstrom R.C., Curren R.D., Yang L.L., Harris C.C., Genotoxicity of formaldehyde in cultured human bronchial fibroblasts, Science, 228, pp. 89-90, (1985)

[54]

Grandjean P, Andersen O, Nielsen G.D., Carcinogenicity of occupational nickel exposures: An evaluation of the epidemiological evidence, Am. J. Ind. Med., 13, pp. 193-209, (1988)

[55]

Greenblatt M, Formaldehyde toxicity: A review of recent research and regulatory changes, Lab. Med., 19, pp. 425-428, (1988)

[56]

Hahon N, Castranova V, Interferon production in rat type II pneumocytes and alveolar macrophages, Exp. Lung Res., 15, pp. 429-445, (1989)

[57]

Hamada J-I, Takeichi N, Kobayashi H, Metastatic capacity and intercellular communication between normal cells and metastatic cell clones derived from rat mammary carcinoma, Cancer Res., 48, pp. 5129-5132, (1988)

[58]

Hamaguchi M, Hanafusa H, Localization of major potential substrates of p60 kinase in the plasma membrane, Oncogene Res., 4, pp. 29-37, (1989)

[59]

Harris C.C., Willey J.C., Saladino A.J., Grafstrom R.C., Effects of tumor promoters, aldehydes, peroxides, and tobacco smoke condensate on growth and differentiation of cultures normal and transformed human bronchial cells, Cocarcinogene-sis—A Comprehensive Survey, pp. 159-171, (1985)

[60]

Harris H, Bramwell M.E., The suppression of malignancy by terminal differentiation: Evidence from hybrids between tumor cells and keratinocytes, J. Cell Sci., 87, pp. 383-388, (1987)

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