title: p53 expression in normal versus transformed mammalian cells.
abstract: To answer the question whether the level of p53 expression also reflects the status of a cell, with reference to transformation and genome stability, we have examined, by immunocytochemistry, the presence of p53 protein in a number of cell types including human diploid cells, Chinese hamster embryonal cells at different passages and gene amplified and/or transformed Chinese hamster cell lines. Primary human fibroblasts at early passage (LEO) and an established, non transformed, Chinese hamster cell line at early passage (CHEF/18) did not show any detectable p53 expression, either nuclear or cytoplasmic. All transformed human (Raji) and Chinese hamster cell lines (CHO, V79, V79/B7) showed a nuclear expression of p53, although at different intensities. Two cell lines selected from V79/B7 for their resistance to phosphonacetyl-L-aspartate or methotrexate and previously shown to bear gene amplification, showed p53 expression. In PALA L cells p53 expression was nuclear as in other positive cell lines tested, while in MTX M cells it was cytoplasmic. CHEF/18 cells at late passage in culture showed the typical behaviour of transformed cells and p53 was detected in several cells. Moreover, when transformed CHO cells were treated with compounds known to induce reverse transformation, both the disappearance of hallmarks of transformed phenotype and p53 reduction were observed. These results indicate a strong association within the same cell type between p53 expression and transformed status.
authors.affiliation: CSTA-Mutagenesis Laboratory, National Institute for Research on Cancer, Genoa, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Moro
authors.forename: L
authors.initials: L
authors.lastname: Ottaggio
authors.forename: S
authors.initials: S
authors.lastname: Bonatti
authors.forename: M
authors.initials: M
authors.lastname: Simili
authors.forename: M
authors.initials: M
authors.lastname: Miele
authors.forename: S
authors.initials: S
authors.lastname: Bozzo
authors.forename: A
authors.initials: A
authors.lastname: Abbondandolo
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D000970:Antineoplastic Agents / Q000633:toxicity; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000633:toxicity; D002051:Burkitt Lymphoma; D016466:CHO Cells; D002460:Cell Line; D002471:Cell Transformation, Neoplastic; D002478:Cells, Cultured; D002772:Cholera Toxin / Q000494:pharmacology; D006224:Cricetinae; D004351:Drug Resistance; D004622:Embryo, Mammalian; D015870:Gene Expression; D016158:Genes, p53; D006801:Humans; D007150:Immunohistochemistry; D007739:L Cells; D008214:Lymphocytes / Q000166:cytology / Q000378:metabolism*; D008727:Methotrexate / Q000633:toxicity; D051379:Mice; D010746:Phosphonoacetic Acid / Q000031:analogs & derivatives / Q000633:toxicity; D012016:Reference Values; D013806:Theophylline / Q000494:pharmacology; D014407:Tumor Cells, Cultured; D016159:Tumor Suppressor Protein p53 / Q000032:analysis / Q000096:biosynthesis*
chemical_list: D000911:Antibodies, Monoclonal; D000970:Antineoplastic Agents; D016159:Tumor Suppressor Protein p53; D001224:Aspartic Acid; C013195:sparfosic acid; D002772:Cholera Toxin; D013806:Theophylline; D010746:Phosphonoacetic Acid; D008727:Methotrexate