Molecular mechanisms of mouse skin tumor promotion.
Molecular mechanisms of mouse skin tumor promotion.
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DOI：
10.3390/cancers2020436
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发表时间：
2010
期刊：
影响因子：
5.2
通讯作者：
Fischer SM
中科院分区：
文献类型：
--
作者：
Rundhaug JE;Fischer SM
促进皮肤癌的发生涉及多个分子机制。通过直接激活有丝分裂信号通路或间接地对慢性创伤和/或炎症做出反应，或由于终末分化受阻或对凋亡的抵抗而诱导持续的增殖和表皮增生是允许DNA突变的起始细胞克隆扩增形成皮肤肿瘤所必需的。有丝分裂途径包括表皮生长因子受体激活和Ras/Raf/丝裂原活化蛋白激酶信号转导。慢性炎症导致炎症细胞分泌生长因子和细胞因子，如肿瘤坏死因子-α和白介素2，以及产生活性氧物种，所有这些都可以刺激增殖。这些通路的持续激活会导致肿瘤的发生。
Multiple molecular mechanisms are involved in the promotion of skin carcinogenesis. Induction of sustained proliferation and epidermal hyperplasia by direct activation of mitotic signaling pathways or indirectly in response to chronic wounding and/or inflammation, or due to a block in terminal differentiation or resistance to apoptosis is necessary to allow clonal expansion of initiated cells with DNA mutations to form skin tumors. The mitotic pathways include activation of epidermal growth factor receptor and Ras/Raf/mitogen-activated protein kinase signaling. Chronic inflammation results in inflammatory cell secretion of growth factors and cytokines such as tumor necrosis factor-α and interleukins, as well as production of reactive oxygen species, all of which can stimulate proliferation. Persistent activation of these pathways leads to tumor promotion.