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Please use this identifier to cite or link to this item: http://hdl.handle.net/10373/1165

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Title: Nothing in excess - lessons learned from the expression of high-mobility group proteins type A in non-cancer and cancer cells
Authors: Petkova, Rumena
Tummala, Hemanth
Zhelev, Nikolai Z.
Affiliation: University of Abertay Dundee. Scottish Informatics, Mathematics, Biology and Statistics Centre
Keywords: HMGA
Cancer
Insulin resistance
Metabolic syndrome
Oxidative DNA damage
Issue Date: Nov-2011
Publisher: Diagnosis Press
Type: Journal Article
Refereed: peer-reviewed
Rights: This is the published version of this article. Reproduced with permission from the publisher. Published version (c)Diagnosis Press, available from http://dx.doi.org/10.5504/bbeq.2011.0102
Citation: Petkova, R., Tummala, H. and Zhelev, N. 2011. Nothing in excess - lessons learned from the expression of high-mobility group proteins type A in non-cancer and cancer cells. Biotechnology & Biotechnological Equipment. 25(4): pp.2572-2575. Available from http://dx.doi.org/10.5504/bbeq.2011.0102
Abstract: High-mobility group A (HMGA) proteins are major transcription regulators which are abundantly and ubiquitously expressed in undifferentiated cells but present at a low level in somatic cells of adult organisms. Up-regulation of HMGA expression is a frequent finding in cancer, either via direct stimulation of expression by constitutively expressed proto-oncogenic factors such as MYC and JUN or by rearrangements rendering the expression of the HMGA proteins not suppressible by inhibitory factors such as miRNAs. Rearrangements of the HMGA genomic loci resulting in disabling of the control mechanisms of their expression are often seen in tumours of various origin. A direct relationship between the level of expression of HMGA in mitochondria and the level of accumulation of oxidative damage in cancer cells has been recently noted. On the other hand, mammalian cells deficient in HMGA1 expression are also deficient in utilization of glucose and show the impairment in expression of the insulin receptor and the high levels of oxidative damage of DNA characteristic of diabetes type 2 and the related condition metabolic syndrome. Insulin resistance and metabolic syndrome could be viewed as a premalignant state in which DNA damage is slowly accumulating until the repair machinery of the cell cannot withstand the constant oxidative barrage and surrenders to neoplastic transformation.
URI: http://hdl.handle.net/10373/1165
ISSN: 1310-2818
Appears in Collections:SIMBIOS Collection
Science Engineering & Technology Collection

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