Cutaneous wound healing through paradoxical MAPK activation by BRAF inhibitors.
作者： Helena Escuin-Ordinas , Shuoran Li , Michael W. Xie , Lu Sun , Willy Hugo
DOI: 10.1038/NCOMMS12348
关键词: Wound healing 、 Mitogen-activated protein kinase kinase 、 Protein kinase A 、 Cancer research 、 Medicine 、 Kinase 、 Vemurafenib 、 MEK inhibitor 、 Melanoma 、 MAPK/ERK pathway
摘要: BRAF inhibitors are highly effective therapies for the treatment of BRAF(V600)-mutated melanoma, with main toxicity being a variety hyperproliferative skin conditions due to paradoxical activation mitogen-activated protein kinase (MAPK) pathway in wild-type cells. Most these changes improve when MEK inhibitor is co-administered, as it blocks MAPK activation. Here we show how vemurafenib accelerates wound healing by inducing proliferation and migration human keratinocytes through extracellular signal-regulated (ERK) phosphorylation cell cycle progression. Topical two wound-healing mice models cutaneous activation; addition (MEK) reverses benefit vemurafenib-accelerated healing. The same dosing regimen topical does not increase incidence squamous carcinomas mice. Therefore, may have clinical applications accelerating wounds.
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