The UC San Diego School of Medicine on Thursday released a study that researchers said upsets the longstanding belief a group of enzymes promotes the growth of cancerous tumors and explains the failure of some attempts to develop an anti-cancer drug.
“Inhibiting PKC has so far proved not only an unsuccessful strategy in a number of cancer clinical trials, but its addition to chemotherapy has resulted in decreased response rates in patients,” said Alexandra Newton, a professor of pharmacology and the study’s principal investigator.
“Given our results, this isn’t surprising,” Newton said. “Our findings suggest therapeutic strategies need to go the other way and target ways to restore PKC activity, not inhibit it. This is contrary to the current dogma.”
Researchers used live cell imaging to reach their conclusions, after they witnessed a majority of cancerous mutations reduced or abolished PKC activity, according to UCSD. The mutations impeded signal binding, prevented correct structuring of the enzyme, or impaired their function as a catalyst of cell activity.
When PKC was restored in the genome of a colon cancer cell line, tumor growth in a mouse model was reduced, demonstrating that normal activity of the enzyme inhibits cancer.
The researchers think that PKC represses signals from genes that can cause normal cells to become cancerous. If that kind of gene is allowed to send its signals, tumors grow.
Scientists with the Salk Institute, Harvard Medical School and University of Manchester in England participated in the study, funded by the National Institutes of Health, James S. McDonnell Foundation, UCSD Graduate Training Program in Cellular and Molecular Pharmacology, the National Science Foundation Graduate Research Fellowship and Cancer Research UK.
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