PubMed · 10278638
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T Baurer. The asbestos problem.. https://pubmed.ncbi.nlm.nih.gov/10278638/
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Although Betaig-h3 gene has been suggested to modulate cell adhesion and tumor formation, its physiological functions are not well understood. Using human papillomavirus immortalized human bronchial epithelial (BEP2D) cells, we found that Betaig-h3 expression was markedly decreased in asbestos-induced tumorigenic cells. Fusion of tumorigenic and control BEP2D cells resulted in the recovery of Betaig-h3 gene expression to control level and the loss of tumorigenic phenotype. Furthermore, ectopic expression of Betaig-h3 gene in asbestos-induced tumorigenic cells inhibited cell growth in vitro, anchorage independent phenotype, as well as tumorigenicity in nude mice. Betaig-h3 gene is ubiquitously expressed in various normal human tissues, with the exception of the brain, where there is little or no expression. In contrast, there was a decrease or absence in expression of the Betaig-h3 gene in 14 human tumor cell lines of diverse histological types examined, when compared with normal human cells or tissues. The result strongly suggests that loss of Betaig-h3 expression is a frequent event in human cancer and causally related to acquisition of tumorigenic phenotype in asbestos-treated BEP2D cells.
Asbestos is a well-known toxin and lung carcinogen. Epidemiologic studies have established tobacco smoke and asbestos exposures synergistically interact to enhance lung cancer risk. The biologic mechanism responsible for this interaction has been the subject of considerable debate. Studies have suggested that asbestos may act as a carcinogen by generating free radical and reactive oxygen species, by inducing tissue injury and subsequent cellular growth, via large-scale chromosome loss and by enhancing delivery of tobacco carcinogens to the respiratory epithelium. Recent molecular epidemiologic approaches further suggest that asbestos enhances the mutagenicity of tobacco carcinogens and that it acts, at least in part, independent of the tissue damage responsible for fibrosis.
We evaluated the frequency of micronuclei (MN) in peripheral blood lymphocytes of patients with pleural malignant mesotelioma (MM), lung cancer, benign respiratory diseases, and healthy controls. A significant increased frequency of MN was observed in patients with MM in comparison with all the other groups (median, 11.4 binucleated MN/1000 binucleated cells versus 5.1, 6.1, and 6.2, respectively). No association was found between MN and asbestos exposure. Recently, genetic susceptibility associated with asbestos exposure has been recognized in the development of MM. The presence of high frequency of MN in peripheral blood lymphocytes of patients with MM could represent a useful index of individual susceptibility to this tumor.