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Mutant p53 protein expression and antioxidant status deficiency in breast cancer
It is well recognized that cancers develop and grow as a result of disordered function of tumor suppressor genes and oncogenes, which may be exploited for screening purposes. Extensive evidence indicated tumor suppressor protein p53 as candidate marker for mutation identification. We have investigat...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Leibniz Research Centre for Working Environment and Human Factors
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4464499/ https://www.ncbi.nlm.nih.gov/pubmed/26417293 |
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author | Milicevic, Zorka Kasapovic, Jelena Gavrilovic, Ljubica Milovanovic, Zorka Bajic, Vladan Spremo-Potparevic, Biljana |
author_facet | Milicevic, Zorka Kasapovic, Jelena Gavrilovic, Ljubica Milovanovic, Zorka Bajic, Vladan Spremo-Potparevic, Biljana |
author_sort | Milicevic, Zorka |
collection | PubMed |
description | It is well recognized that cancers develop and grow as a result of disordered function of tumor suppressor genes and oncogenes, which may be exploited for screening purposes. Extensive evidence indicated tumor suppressor protein p53 as candidate marker for mutation identification. We have investigated mutant p53 protein expression in human breast tumors in relation to antioxidant status deficiency. The study included 100 breast cancer patients. p53 protein expression was evaluated by Western blot assay and immunostaining using a CM-1, DO-7 and Pab240 antibodies. Antioxidant parameters and lipid peroxidation were estimated by biochemical analyses. Western blotting with epitopespecific monoclonal antibody Pab240 strongly suggests that nuclear extracts from breast cancer cells express mutant forms of p53. It is of interest that the mutant forms of p53 overexpression in conjunction with the appearance of nuclear bodies are observed in highly aggressive carcinomas. Expression of isoform Δp53 (45 kDa) and isoform of ~ 29 kDa were more common in cases with LN metastasis. These studies point out the molecular consequences of oxidative stress (lipid peroxides, LP, p<0.001) and antioxidant status deficiency (copper, zinc superoxid dismutase, SOD, p<0.001; catalase, CAT, p<0.01; glutathione reductase, GR, p<0.001; glutathione, GSH, p<0.05) and indicate the importance of p53 mutation as the commonest genetic alteration detected in breast cancer cells. The expression of mutant p53 is correlated to increased lipid peroxides (0.346, p<0.05 ) and lowered antioxidant activity of CAT (- 0.437, p<0.01) in the breast cancer patients. |
format | Online Article Text |
id | pubmed-4464499 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Leibniz Research Centre for Working Environment and Human Factors |
record_format | MEDLINE/PubMed |
spelling | pubmed-44644992015-09-28 Mutant p53 protein expression and antioxidant status deficiency in breast cancer Milicevic, Zorka Kasapovic, Jelena Gavrilovic, Ljubica Milovanovic, Zorka Bajic, Vladan Spremo-Potparevic, Biljana EXCLI J Original Article It is well recognized that cancers develop and grow as a result of disordered function of tumor suppressor genes and oncogenes, which may be exploited for screening purposes. Extensive evidence indicated tumor suppressor protein p53 as candidate marker for mutation identification. We have investigated mutant p53 protein expression in human breast tumors in relation to antioxidant status deficiency. The study included 100 breast cancer patients. p53 protein expression was evaluated by Western blot assay and immunostaining using a CM-1, DO-7 and Pab240 antibodies. Antioxidant parameters and lipid peroxidation were estimated by biochemical analyses. Western blotting with epitopespecific monoclonal antibody Pab240 strongly suggests that nuclear extracts from breast cancer cells express mutant forms of p53. It is of interest that the mutant forms of p53 overexpression in conjunction with the appearance of nuclear bodies are observed in highly aggressive carcinomas. Expression of isoform Δp53 (45 kDa) and isoform of ~ 29 kDa were more common in cases with LN metastasis. These studies point out the molecular consequences of oxidative stress (lipid peroxides, LP, p<0.001) and antioxidant status deficiency (copper, zinc superoxid dismutase, SOD, p<0.001; catalase, CAT, p<0.01; glutathione reductase, GR, p<0.001; glutathione, GSH, p<0.05) and indicate the importance of p53 mutation as the commonest genetic alteration detected in breast cancer cells. The expression of mutant p53 is correlated to increased lipid peroxides (0.346, p<0.05 ) and lowered antioxidant activity of CAT (- 0.437, p<0.01) in the breast cancer patients. Leibniz Research Centre for Working Environment and Human Factors 2014-06-23 /pmc/articles/PMC4464499/ /pubmed/26417293 Text en Copyright © 2014 Milicevic et al. http://www.excli.de/documents/assignment_of_rights.pdf This is an Open Access article distributed under the following Assignment of Rights http://www.excli.de/documents/assignment_of_rights.pdf. You are free to copy, distribute and transmit the work, provided the original author and source are credited. |
spellingShingle | Original Article Milicevic, Zorka Kasapovic, Jelena Gavrilovic, Ljubica Milovanovic, Zorka Bajic, Vladan Spremo-Potparevic, Biljana Mutant p53 protein expression and antioxidant status deficiency in breast cancer |
title | Mutant p53 protein expression and antioxidant status deficiency in breast cancer |
title_full | Mutant p53 protein expression and antioxidant status deficiency in breast cancer |
title_fullStr | Mutant p53 protein expression and antioxidant status deficiency in breast cancer |
title_full_unstemmed | Mutant p53 protein expression and antioxidant status deficiency in breast cancer |
title_short | Mutant p53 protein expression and antioxidant status deficiency in breast cancer |
title_sort | mutant p53 protein expression and antioxidant status deficiency in breast cancer |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4464499/ https://www.ncbi.nlm.nih.gov/pubmed/26417293 |
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