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A CROSSTALK BETWEEN PROGESTERONE RECEPTOR B AND P53 ALTERS THE METABOLIC REPROGRAMMING IN BREAST CANCER CELL LINES
Vol 32, Issue 4S1, 2018
Abstract
Progesterone-Receptor (PR) is good prognostic marker for breast cancer patients. The effects ofProgesterone on its target tissues are mediated by the Progesterone Receptors (PR-A and PR-B). Inbreast tumors from patients with poor prognosis, a loss of PR-B occurs suggesting a protective role ofPR-B in breast cancer. The molecular mechanisms of PR-B–protective effects are still to be defined.Recently, we reported in breast cancer cells a novel functional interplay between PR-B and PTEN inmodulating autophagy, which is retained a way to reprogram cellular metabolism activating oncogenesand inactivating tumor suppressors. Among them, the p53 tumor suppressor gene has emerged asimportant mediator of energy metabolism. To deepen the PR-B anticancer role and given the relationshipbetween autophagy and cellular metabolism, we investigated a role for OHPg/PR-B signaling throughp53 in altering metabolic reprogramming of breast cancer cells.
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Supporting Agencies
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Medical Genetics, University of Torino Medical School, Italy
Department of Biomedical, Surgical and Dental Sciences, University of Milan, Italy