Modulation of protein kinase C in antitumor treatment

摘要: PKC isoenzymes were found to be involved in proliferation, antitumor drug resistance and apoptosis. Therefore, it has been tried exploit as a target for treatment. alpha activity was elevated, example, breast cancers malignant gliomas, whereas seems underexpressed many colon cancers. So can expected that inhibition of will not show similar all tumors. In some tumors essential inhibit reduce growth. However, tumor proliferation may an advantage induce this case activation delta should achieved. The situation is complicated by the facts bryostatin leads later downmodulation inhibitors available date are specific one isoenzyme. For these reasons, modulation led contradicting results. Despite problems, modulators such miltefosine, bryostatin, safingol, CGP41251 UCN-01 used clinic or clinical evaluation. question whether major only compounds, because they also interfere with other targets. Oncogenes growth factors cell survival, however, apoptosis, depending on type conditions which cells grown. participates signalling pathways cross-talks. Induction apoptosis dependent additional factors, p53, bcl-2, mdm2, etc. there results Similar controversial data have reported about MDR1-mediated multidrug resistance. At present alone without direct interaction PGP lead successful reversal PGP-mediated efflux. One possibility improve chemotherapy would combine established drugs PKC. here very contrasting obtained. Many indicate inhibition, others, enhances antiproliferative anticancer drugs. problem exact functions different clear at present. further investigations into role complex interacting essential. It challenge future reveal improvement cancer therapy.