Here, we test whether the oncoprotein RET/PTC could be responsible for this effect, since RET/PTC rearrangements are quite prevalent in PTC and RET/PTC activates PLCgamma, an upstream modulator of PKCs.     ///    "Activation was restricted to PKCepsilon, as acute expression of RET/PTC did not change the subcellular distribution of other PKC isozymes expressed in PCCL3 cells. "    ///    Acute expression of RET/PTC induces isozyme-specific activation and subsequent downregulation of PKCepsilon in PCCL3 thyroid cells..     ///    Prolonged RET/PTC expression (2-6 days) produced an isozyme-specific change in PKCepsilon subcellular localization and a decrease in total PKCepsilon levels.     ///    "At 3 h after induction of RET/PTC1 or RET/PTC3 expression, there was evidence of PKCepsilon activation. "    ///    "However, downregulation of total PKCepsilon levels was only partially prevented by expression of RET/PTC(Y541F). "    ///    "Based on our previous observation that PCCL3 cells expressing a dominant-negative PKCepsilon are also markedly resistant to apoptosis, we propose that selective downregulation of PKCepsilon following prolonged RET/PTC activation promotes cell survival and clonal expansion.. "    ///    Cells with decreased PKCepsilon following prolonged expression of RET/PTC were relatively resistant to doxorubicin-induced apoptosis. 