Differential sensitivity of RIP3-proficient and deficient murine fibroblasts to camptothecin anticancer drugs

Dear Editor, Receptor-interacting protein 3 （RIP3） is a serine/threonine protein kinase, which has extensive substrates including its cognate kinase RIP1 and multiple metabolic enzymes involving oxidative phosphorylation. RIP3 has been shown to be essential for development, immunity and some physiological or pathophysiological responses to exogenous and endoge- nous stimuliI3-sl. In 2009, three groups independently reported that RIP3 acted as a molecular switch between apoptosis and necrosis （also called as necroptosis）E6-81. Specifically, RIP3 could turn tumor necrosis factor （TNF）-induced cell death from apoptosis to necrosis[61. Most of small-molecule antican- cer drugs elicit their anticancer effects via apoptotic induc- tion. However, it is unclear whether RIP3 affects the cellular sensitivity to small-molecule anticancer drugs.