Journal
CELL
Volume 141, Issue 4, Pages 717-727Publisher
CELL PRESS
DOI: 10.1016/j.cell.2010.04.021
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Funding
- National Health and Medical Research Council of Australia (NHMRC) [402761]
- Australian Cancer Research Foundation
- Melanoma and Skin Cancer Research Institute, University of Sydney
- Melanoma Foundation of the University of Sydney
- Department of Anatomical Pathology at the Royal Prince Alfred Hospital
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Induction of senescence permanently restricts cellular proliferation after oncogenic stimulation thereby acting as a potent barrier to tumor development. The relevant effector proteins may therefore be fundamental to cancer development. A recent study identified IGFBP7 as a secreted factor mediating melanocyte senescence induced by oncogenic B-RAF, which is found commonly in cutaneous nevi. In contrast to the previous report, we demonstrate that B-RAF signaling does not induce IGFBP7 expression, nor the expression of the IGFBP7 targets, BNIP3L, SMARCB1, or PEA15, in human melanocytes or fibroblasts. We also found no correlation between B-RAF mutational status and IGFBP7 protein expression levels in 22 melanoma cell lines, 90 melanomas, and 46 benign nevi. Furthermore, using a lentiviral silencing strategy we show that B-RAF induces senescence in melanocytes and fibroblasts, irrespective of the presence of IGFBP7. Therefore, we conclude that the secreted protein IGFBP7 is dispensable for B-RAF (V600E)-induced senescence in human melanocytes.
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