C/EBPβ deletion in oncogenic Ras skin tumors is a synthetic lethal event
Cell Death & Disease, 9(11).
By: Z. Messenger, J. Hall, D. Jima, J. House, H. Tam, D. Tokarz, R. Smart*
MeSH headings : 9,10-Dimethyl-1,2-benzanthracene / administration & dosage; Animals; Apoptosis / drug effects; Apoptosis / genetics; CCAAT-Enhancer-Binding Protein-beta / deficiency; CCAAT-Enhancer-Binding Protein-beta / genetics; Cell Differentiation; Cell Transformation, Neoplastic / genetics; Cell Transformation, Neoplastic / metabolism; Cell Transformation, Neoplastic / pathology; Gene Expression Regulation, Neoplastic; Genes, Lethal; Keratinocytes / drug effects; Keratinocytes / metabolism; Keratinocytes / pathology; Mice; Mice, Knockout; Receptors, Death Domain / genetics; Receptors, Death Domain / metabolism; Signal Transduction; Skin / drug effects; Skin / metabolism; Skin / pathology; Skin Neoplasms / chemically induced; Skin Neoplasms / genetics; Skin Neoplasms / metabolism; Skin Neoplasms / pathology; Tetradecanoylphorbol Acetate / administration & dosage; Tetradecanoylphorbol Acetate / analogs & derivatives; Tumor Suppressor Protein p53 / genetics; Tumor Suppressor Protein p53 / metabolism; ras Proteins / genetics; ras Proteins / metabolism
TL;DR:
The results show that oncogenic Ras tumors display a significant DNA damage/replicative stress phenotype and these tumors have acquired a dependence on C/EBPβ for their survival, making it a promising target for future potential anticancer therapies.
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