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Simultaneous suppression of progression marker genes in the highly malignant human melanoma cell line BLM after transfection with the adenovirus-5 E1A gene.

Biochemical and Biophysical Research Communications

Tumor Markers, Biological, genetics, Animals, Gene Expression Regulation, Neoplastic, Adenoviruses, Human, Genes, Viral, Humans, Interleukin-6, biosynthesis, Melanoma, immunology, secondary, Mice, Mice, Nude, Suppression, Genetic, Transfection, Tumor Cells, Cultured, Adenovirus E1A Proteins

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      The highly metastatic human melanoma cell line BLM was transfected with the E1A or E1A + E1B regions of adenovirus 5 (Ad5). A series of progression markers, correlated with the malignant phenotype of parental BLM (including calcyclin, thymosin beta 10, plasminogen activator inhibitors types 1 and 2, urokinase type and tissue type plasminogen activators, vimentin, tissue type transglutaminase, and interleukin-6), was collectively repressed in the transfectants, whereas several control genes were not affected or even induced. The apparently coordinate repression of a set of markers by the same regulator gene, Ad5 E1A in this case, suggests the existence of one pathway under the control of a main switch and predicts that one or more as yet unidentified cellular master genes normally exert this function. A reduced oncogenicity was observed after subcutaneous inoculation of the E1A transfectants into nude mice and provides additional evidence in support of a tumor suppressor function of Ad5 E1A.

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