RIP3 expression induces a death profile change in U2OS osteosarcoma cells after 5-ALA-PDT.

摘要: Background and Objective: The receptor-interacting protein 3 (RIP3) has recently been outlined as a key necrosis mediator but is also thought to participate in the regulation of apoptosis. aim this study compare cell death profile induced by 5-aminolevulic acid (5-ALA)-mediated photodynamic therapy (PDT) RIP3-deficient line U2OS cells which expression RIP3 was restored. Materials Methods: RIP3-expressing (RIP3-U2OS) were obtained after transfection antibiotic selection. Wild type RIP3-U2OS treated 5-ALA-PDT. Overall viability evaluated different parameters characteristic apoptosis, autophagy, studied. Results: Surprisingly, survival higher compared that wild cells. In addition, decreased zVADfmk pre-treatment. A cleavage caspase-3, 7, 8, 9, PARP detected these cells, pointing out activation caspase-dependent parallel, thrust autophagy clearly identified RIP3U2OS Conversely, exhibited lower level than types. Interestingly, necrostatin-1 efficiently not Conclusion: Expression led better change response PDT. apoptotic autophagic pathways up-regulated However, induction weaker context, likely play protective role against PDT-induced allow This work highlights important played pathway, although modalities are still widely unknown. Lasers Surg. Med. 43:557– 564, 2011. 2011 Wiley-Liss, Inc.