Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The identification of genes involved in the process of neoplastic transformation is essential for analyzing the progression of breast cancer when induced by endogenous and exogenous agents, among which are the estrogens and the organophosphorous pesticides, respectively. It is important to consider the impact of such substances when they are present in combination. In vitro experimental models are needed in order to understand breast carcinogenesis. The aim of this work was to examine the effect of 17beta estradiol (estrogen) combined with either malathion or parathion on the transformation of human breast epithelial cells in vitro. Results showed that estrogen combined with either malathion or parathion altered cell proliferation and induced cell transformation as well as exhibited significant invasive capabilities as compared to the control MCF-10F cell line. Several genes were up-regulated by the effect of all of the treatments, such as the cyclins, cyclin D1 and cyclin-dependent kinase 4, IGFBP3 and IGFBP5, and keratin 18. The c-Ha-ras oncogene was up-regulated by the effect of malathion alone and with the combination of estrogen and either malathion or parathion. The DVL1 gene was up-regulated only with malathion alone and the combination of parathion with estrogen. Expression of the HSP 27, MCM2 and TP53 inducible protein 3 genes was up-regulated with malathion alone and with the combination of estrogen and either malathion or parathion while TP53 (Li-Fraumeni syndrome) was up-regulated by estrogen alone and malathion alone. Thus, we suggest that pesticides and estrogens affect human breast cells inducing molecular changes indicative of transformation.
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PMID:Cancer genes induced by malathion and parathion in the presence of estrogen in breast cells. 1820 94

We have studied the effect of acute L-glutamine deprivation on the expression oftumor protein 53 (TP53)-related genes such as TOPORS (topoisomerase I binding, arginine/serine-rich, E3 ubiquitin protein ligase), TP53BPI (TP53 bindingprotein 1), TP53TG1 (TP53 inducible gene 1), SESN1 (p53 regulatedPA26 nuclear protein), NME6 (NME/NM23 nucleoside diphosphate kinase 6), and ZMAT3 (zinc finger Matrin-type 3) in glioma cells with ERN1 knockdown. It was shown that blockade of ERN1 finction in U87 glioma cells is induced the expression of RYBP and SESN1 genes, but decreased the expression of TP53BP1, TP53TG1, TOPORS, NME6, genes. Moreover, the expression levels ofRYBPI SESN1, TP53BP1, and ZMAT3 genes is increased in control glioma cells by L-glutamine deprivation condition but blockade of ERN1 signaling enzyme function significantly enhances this effect on the expression all of these genes. At the same time, the ERN1 knockdown eliminates the response TP53TG1 and TOPORS genes to L-glutamine deprivation condition. Results of this investigation clearly demonstrate that the expression most of genes encoding TP53-related factors depends upon acute L-glutamine deprivation condition as well as upon ERN1, the major signaling system of the endoplasmic reticulum stress.
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PMID:Acute L-glutamine deprivation affects the expression of TP53-related protein genes in U87 glioma cells. 2533 30