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1

The putative role of cell adhesion molecules and N-Cam in particular in tumor formation and spreading

100%
Zeromski J.
Folia Histochemica et Cytobiologica. Supplement
|
2001
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tom 39
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nr 1
2

The role of ras genes in the neoplasmic transformation in animals

86%
Rotkiewicz T., Slodki S., Otrocka-Domagala I.
Polish Journal of Veterinary Sciences
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2004
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tom 07
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nr 1
We can distinguish three kinds of ras genes i.e. H-ras, K-ras and N-ras, which are rated as ras-protooncogenes. The point mutations within ras genes are frequently detected in human malignancies and in experimentally induced tumors in animals. The aim of this article is to review briefly current research on the role and the frequency oíras gene mutational activation in naturally occurring animal tumors. The present studies show that the mutational activation of ras genes at the hot-spot loci in codons 12, 13 and 61 is apparently rare and does not perform an important role in the pathogenesis of naturally occurring tumors in animals. However, we cannot be sure if the mutational activation of ras genes occurs most often, but in other functional areas of these genes, or if there are other mechanisms involved in their activation.
3

Expression and hypoxia-responsiveness of 6-phosphofructo-2-kinase-fructose-2,6-bisphosphatase 4 in mammary gland malignant cell lines

72%
Minchenko O. H., Opentanova I. L., Ogura T., Minchenko D. O., Komisarenko S. V., Caro J., Esumi H.
Acta Biochimica Polonica
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2005
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tom 52
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nr 4
Recently, we have shown that PFKFB4 gene which encodes the testis isoenzyme of PFKFB is also expressed in the prostate and hepatoma cancer cell lines. Here we have studied expression and hypoxic regulation of the testis isoenzyme of PFKFB4 in several malignant cell lines from a female organ - the mammary gland. Our studies clearly demonstrated that PFKFB4 mRNA is also expressed in mammary gland malignant cells (MCF-7 and T47D cell lines) in normoxic conditions and that hypoxia strongly induces it expression. To better understand the mechanism of hypoxic regulation of PFKFB4 gene expression, we used dimethyloxalylglycine, a specific inhibitor of HIF-1α hydroxylase enzymes, which strongly increases HIF-1α levels and mimics the effect of hypoxia. It was observed that PFKFB4 expression in the MCF7 and T47D cell lines was highly responsive to dimethyloxalylglycine, suggesting that the hypoxia responsiveness of PFKFB4 gene in these cell lines is regulated by HIF-1 proteins. Moreover, desferrioxamine and cobalt chloride, which mimic the effect of hypoxia by chelating or substituting for iron, had a similar stimulatory effect on the expression of PFKFB mRNA. In other mammary gland malignant cell lines (BT549, MDA-MB-468, and SKBR-3) hypoxia and hypoxia mimics also induced PFKFB4 mRNA, but to variable degrees. The hypoxic induction of PFKFB4 mRNA was equivalent to the expression of PFKFB3, Glut1, and VEGF, which are known HIF-1-dependent genes. Hypoxia and dimethyloxalylglycine increased the PFKFB4 protein levels in all cell lines studied except MDA-MB-468. Through site-specific mutagenesis in the 5'-flanking region of PFKFB4 gene the hypoxia response could be limited. Thus, this study provides evidence that PFKFB4 gene is also expressed in mammary gland cancer cells and strongly responds to hypoxia via an HIF-1α dependent mechanism. Moreover, the PFKFB4 and PFKFB3 gene expression in mammary gland cancer cells has also a significant role in the Warburg effect which is found in all malignant cells.
4

Mitochondrial DNA mutations in human neoplasia

58%
Czarnecka A. M., Golik P., Bartnik E.
Journal of Applied Genetics
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2006
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tom 47
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nr 1
Many models of tumour formation have been put forth so far. In general they involve mutations in at least three elements within the cell: oncogenes, tumour suppressors and regulators of telomere replication. Recently numerous mutations in mitochondria have been found in many tumours, whereas they were absent in normal tissues from the same individual. The presence of mutations, of course, does not prove that they play a causative role in development of neoplastic lesions and progression; however, the key role played by mitochondria in both apoptosis and generation of DNA-damaging reactive oxygen species might indicate that the observed mutations contribute to tumour development. Recent experiments with nude mice have proven that mtDNA mutations are indeed responsible for tumour growth and exacerbated ROS production. This review describes mtDNA mutations in main types of human neoplasia.
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