Journal
TRENDS IN PHARMACOLOGICAL SCIENCES
Volume 38, Issue 5, Pages 438-447Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tips.2017.02.002
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Funding
- NIH [GM 43154]
- National Cancer Institute [ZIA BC 011691]
- Cancer Research UK
- Cancer Research UK [12936] Funding Source: researchfish
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The discovery in the 1980s that protein kinase C (PKC) is a receptor for the tumor-promoting phorbol esters fueled the dogma that PKC is an oncoprotein. Yet 30+ years of clinical trials for cancer using PKC inhibitors not only failed, but in some instances worsened patient outcome. The recent analysis of cancer-associated mutations, from diverse cancers and throughout the PKC family, revealed that PKC isozymes are generally inactivated in cancer, supporting a tumor suppressive function. In keeping with a bona fide tumor suppressive role, germline causal loss-of-function (LOF) mutations in one isozyme have recently been identified in lymphoproliferative disorders. Thus, strategies in cancer treatment should focus on restoring rather than inhibiting PKC.
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