2013
DOI: 10.18632/aging.100577 View full text |Buy / Rent full text
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Abstract: Normal cells enter a senescent state upon aberrant oncogenic signals and this response inhibits tumor initiation and progression. It is now well admitted that intracellular and membrane localized oncogenes can illicit oncogene induced senescence. However, the effect of mitogenic growth factor on cellular senescence is so far largely unknown. Here we show that normal human dermal fibroblasts display a complex response to Platelet derived growth factor B (PDGFB) expression. Indeed, PDGFB expression induces, in t… Show more

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“…To identify new regulators of senescence, we performed a genetic screen using a shRNA library covering the whole genome in normal human fibroblasts induced to senescence by an oncogenic stress (Vindrieux et al., 2013). We thus obtained a list of genes inducing an escape from OIS when knocked down (Figure S1) and were particularly interested in the SCN9A sodium channel, which has so far never been associated with OIS.…”
Section: Resultsmentioning
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“…To identify new regulators of senescence, we performed a genetic screen using a shRNA library covering the whole genome in normal human fibroblasts induced to senescence by an oncogenic stress (Vindrieux et al., 2013). We thus obtained a list of genes inducing an escape from OIS when knocked down (Figure S1) and were particularly interested in the SCN9A sodium channel, which has so far never been associated with OIS.…”
Section: Resultsmentioning
“…1,2 Platelets are also receiving growing attention in senescence, as platelet-derived growth factor has been reported to induce both senescence and cellular transformation in human fibroblasts; 3 given that senescence plays a key role during oncogenesis and inflammation, 3,4 the role of these anucleated cells is starting to be further investigated. Loss of platelets, due either to decreased survival in the periphery or to reduced production, can occur in several diseases, including thrombocytopenic purpura, acute leukemia, aplastic anaemia, multiple myeloma, HELLP (hemolysis, elevated liver enzymes, low platelets) and Scott (a rare bleeding disorder) syndromes.…”
Section: Introductionmentioning
“…It was reported that PDGF-bR inhibitor imatinib restricted the migration and distribution of collagen-synthesizing cells to wound margins, but did not prevent myofibroblast differentiation [51], highlighting the significance of PDGF-BB signaling for recruitment and functional activities of fibroblasts during the early phases of hypertrophic scars. Interestingly, PDGF-BB was recently found to induce p53-dependent senescence and cellular transformation in human dermal fibroblasts, and this low level of senescence might decrease the transforming ability of PDGF-BB without totally abolishing it [52]. The therapeutic relevance of this finding for hypertrophic scars is completely unknown, but this issue should be carefully considered in developing anti-PDGF therapies for hypertrophic scars, so as to achieve the most favorable effects but avoid the unwanted effects.…”
Section: Platelet-derived Growth Factor Pathwaymentioning