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 physiol...

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Published inActa pharmacologica Sinica Vol. 33; no. 3; pp. 426 - 428
Main Authors He, Jin-xue, Wang, Ying-qing, Feng, Jian-ming, Li, Jia-xin, Xu, Lei, Li, Xiao-hua, Wang, Wei, Huan, Xia-juan, Jiang, Yi, Yu, Bing, Chen, Guang, Miao, Ze-hong
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.03.2012
Nature Publishing Group
Subjects
Animals
Antineoplastic Agents - pharmacology
Apoptosis - drug effects
Apoptosis - genetics
Biomedical and Life Sciences
Biomedicine
Camptothecin - pharmacology
Fibroblasts - drug effects
Fibroblasts - enzymology
Fibroblasts - metabolism
Fibroblasts - pathology
Immunology
Internal Medicine
Letter
letter-to-the-editor
Medical Microbiology
Mice
Necrosis
NIH 3T3 Cells
Pharmacology/Toxicology
Receptor-Interacting Protein Serine-Threonine Kinases - genetics
Receptor-Interacting Protein Serine-Threonine Kinases - metabolism
Vaccine
丝氨酸/苏氨酸蛋白激酶
喜树碱
小鼠
成纤维细胞
抗癌药物
敏感性
缺陷
肿瘤坏死因子
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Summary: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.
Bibliography: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.
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These authors contributed equally to this work.
ISSN:1671-4083
1745-7254
DOI:10.1038/aps.2012.1