Abstract
Activation of AKT signaling pathway and mTOR substrates of kidney tumor tissue occurs by improving AKT, its phosphorylated form, the serine / threonine proteinkinase m-TOR, the exchange regulator glycogen GSK-3-beta and also the inhibitor of 4E-BP1transcription. Increasing the size of primary tumor is followed by increasing the content of therein c-Raf and decreasing the content of phospho-m-TOR. The development of disseminated forms of the disease was associated with a reduction PTEN and phospho-AKT in tumor.
MeSH terms
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Female
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Gene Expression Regulation, Neoplastic
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Glycogen Synthase Kinase 3 beta / genetics*
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Humans
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Kidney Neoplasms / genetics*
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Kidney Neoplasms / pathology
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Male
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Middle Aged
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PTEN Phosphohydrolase / genetics
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Proto-Oncogene Proteins c-akt / genetics*
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Proto-Oncogene Proteins c-raf / genetics
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Signal Transduction / genetics
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TOR Serine-Threonine Kinases / genetics*
Substances
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MTOR protein, human
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Glycogen Synthase Kinase 3 beta
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Proto-Oncogene Proteins c-akt
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Proto-Oncogene Proteins c-raf
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Raf1 protein, human
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TOR Serine-Threonine Kinases
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PTEN Phosphohydrolase
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PTEN protein, human