Abstract
Embryonic and tumour cells are able to protect themselves against various harmful compounds. In human pathology, this phenomenon exists in the form of multidrug resistance (MDR) that significantly deteriorates success of anticancer treatment. Cytochromes P450 (CYPs) play one of the key roles in the xenobiotic metabolism. CYP expression could contribute to resistance of cancer cells to chemotherapy. CYP epoxygenases (CYP2C and CYP2J) metabolize about 20% of clinically important drugs. Besides of drug metabolism, CYP epoxygenases and their metabolites play important role in embryos, normal body function, and tumors. They participate in angiogenesis, mitogenesis, and cell signaling. It was found that CYP epoxygenases are affected by peroxisome proliferator-activated receptor α (PPARα). Based on the results of current studies, we assume that PPARs ligands may regulate CYP2C and CYP2J and in some extent they may contribute to overcoming of MDR in patients with different types of tumours.
Highlights
Embryonic stem cells are equipped with the multiple mechanisms to protect their integrity against potential mutagenic mechanisms associated with inflammation, infection, and dietary toxins
As we described earlier [2], peroxisome proliferatoractivated receptors (PPARs), especially PPARγ, may regulate expression of multidrug resistance (MDR) pumps
The CYP2C subfamily represents about 18% of total adult liver cytochrome P450 content [10]
Summary
Embryonic stem cells are equipped with the multiple mechanisms to protect their integrity against potential mutagenic mechanisms associated with inflammation, infection, and dietary toxins. Because of similarities between embryonic and tumour cells, it is well accepted that embryonic cells could be used as powerful tool to study natural mechanisms of cell protection. Understanding of protection mechanisms of the cells may help overcome multidrug resistance (MDR) in different types of tumours. As we described earlier [2], peroxisome proliferatoractivated receptors (PPARs), especially PPARγ, may regulate expression of MDR pumps. It seems that PPARs affect the expression of ABC transporters but they affect certain enzymes of phase I metabolism of xenobiotics. We suppose that these compounds may contribute to the safe regulation of MDR in cancer treatment
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