Differential response for retinoid treatment for normal and transformed murine mammary cells overexpressing protein kinase C (PKC) isoforms

DIAZ BESSONE; BERARDI; CIRIGLIANO; FLUMIAN; BAL DE KIER JOFFE; TODARO; URTREGER

Washington

Congreso; 104 Annual Meeting of the American Association for Cancer Research; 2013

Some of the most promising signaling pathways for breast cancer treatment include the PKC family, involved in proliferation and apoptosis, and the retinoid system mainly involved in differentiation. In this work we have overexpressed α or δ PKC isoforms in two murine mammary models, a tumor-derived cell line (LM3) and a normal mammary gland-derived line (NMuMG), in order to analyze whether elevated expression of these kinases alter the sensitivity to retinoid treatment. The overexpression of α or δ PKC isozymes did not induce detectable morphological alterations either in LM3 or in NMuMG cell lines. In the transformed cell context, the overexpression of PKCα increased cell proliferation (population doubling time: 14.8±2.3 h vs 21.2±3.1 h in control cells p