Journal
CANCER AND METASTASIS REVIEWS
Volume 20, Issue 1-2, Pages 95-100Publisher
KLUWER ACADEMIC PUBL
DOI: 10.1023/A:1013186430906
Keywords
drug-induced apoptosis; multidrug resistance (MDR); P-glycoprotein (Pgp); protein kinase C (PKC)
Categories
Funding
- NATIONAL CANCER INSTITUTE [R01CA074831, R55CA074831] Funding Source: NIH RePORTER
- NCI NIH HHS [CA 74831] Funding Source: Medline
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The seminal discovery in 1988 that selective protein kinase C (PKC) activators induce multidrug resistance (MDR) in human cancer cells spawned several years of intensive investigations; these studies were primarily directed at the question of whether isozyme-selective PKC antagonism could reverse MDR phenotypes produced in cancer cells by P-glycoprotein and other ATP-binding cassette (ABC) transporters. The first section of this commentary provides a succinct overview of those studies. In the second section, we evaluate why the enthusiasm for studies of the involvement of PKC in transport-related drug resistance is currently diminished, and we offer an assessment of whether the PKC/MDR field should be revisited. The final section of the commentary highlights recent developments in studies of PKC targeting in experimental cancer therapeutics, which continues to be a vibrant field. Highlights include the sensitization of cancer cells to radiation- and drug-induced apoptosis by PKC inhibition.
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