Role of protein kinases in antitumor drug resistance

Clicks: 255
ID: 112093
1970
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Abstract
The activity of several proteins involved in the development of antitumor drug resistance is regulated by protein phosphorylation. These proteins include the mdr-1-encoded P-glycoprotein (Pgp) and topoisomerase II (topo II). The corresponding evidence is reviewed and attempts to modulate multidrug resistance (MDR) by protein kinase C inhibitors are described. The expression of several proteins which are essential in drug resistance is regulated at the transcriptional level, involving protein phosphorylation by members of the protein kinase C (PKC) family, casein kinase II (CKII), and others. These proteins include mdr-1-encoded P-glycoprotein, metallothionein, glutathione S-transferase (GST), dTMP synthase, and the proteins Fos and Jun. The corresponding genes are under positive regulation of ras, which in turn requires the activation of a protein kinase cascade for its function. Protein kinases are therefore potentially useful targets in reducing the expression of proteins involved in the development of multifactorial drug resistance caused by the expression of transforming ras-genes. Attempts to inhibit the ras-induced fos expression by an inhibitor of protein kinase C (ilmofosine) are described. Protein kinase inhibitors are also able to synergistically enhance the cytotoxicity of ds-platinum, which is discussed as resulting from a reduction of PKC-dependent fos expression.
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grunicke1970annalsrole Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors H. Grunicke;J. Hofmann;I. Utz;F. überall;H. Grunicke;J. Hofmann;I. Utz;F. überall;
Journal Annals of hematology
Year 1970
DOI
doi:10.1007/BF01757347
URL
https://link.springer.com/article/10.1007/BF01757347
Keywords
oncology hematology

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