SDF-1α mediates wound-promoted tumor growth in a syngeneic orthotopic mouse model of breast cancer.
SDF-1α mediates wound-promoted tumor growth in a syngeneic orthotopic mouse model of breast cancer.
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DOI：
10.1371/journal.pone.0060919
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Niederhuber JE
中科院分区：
文献类型：
--
作者：
Stuelten CH;Cervoni-Curet FN;Busch JI;Sutton E;Webster JD;Kavalukas SL;Wakefield LM;Barbul A;Niederhuber JE
据报道，急性手术伤口附近的残留肿瘤生长增加;然而，伤口促进肿瘤生长的机制仍然未知。在这里，我们使用了同基因，原位小鼠乳腺癌模型，研究创伤促进肿瘤生长的机制。我们的研究结果表明，转移性小鼠乳腺癌细胞（4 T1）暴露于SDF-1α（在伤口液中增加）导致肿瘤生长增加。创伤和暴露于SDF-1α的4 T1细胞不仅增加了肿瘤生长，而且增加了肿瘤细胞增殖率和基质胶原沉积。相反，用小分子AMD 3100全身抑制SDF-1α信号传导消除了创伤效应，并将细胞增殖、胶原沉积和新血管生成降低至对照动物中观察到的水平。此外，使用不同的小鼠品系，我们可以证明创伤对肿瘤生长和SDF-1α水平的影响是宿主依赖性的，并且在小鼠品系之间存在差异。我们的研究结果表明，伤口促进肿瘤生长是由升高的SDF-1α水平介导的，并表明急性伤口对肿瘤生长的影响取决于宿主背景的预定伤口反应及其预定伤口反应。
Increased growth of residual tumors in the proximity of acute surgical wounds has been reported; however, the mechanisms of wound-promoted tumor growth remain unknown. Here, we used a syngeneic, orthotopic mouse model of breast cancer to study mechanisms of wound-promoted tumor growth. Our results demonstrate that exposure of metastatic mouse breast cancer cells (4T1) to SDF-1α, which is increased in wound fluid, results in increased tumor growth. Both, wounding and exposure of 4T1 cells to SDF-1α not only increased tumor growth, but also tumor cell proliferation rate and stromal collagen deposition. Conversely, systemic inhibition of SDF-1α signaling with the small molecule AMD 3100 abolished the effect of wounding, and decreased cell proliferation, collagen deposition, and neoangiogenesis to the levels observed in control animals. Furthermore, using different mouse strains we could demonstrate that the effect of wounding on tumor growth and SDF-1α levels is host dependent and varies between mouse strains. Our results show that wound-promoted tumor growth is mediated by elevated SDF-1α levels and indicate that the effect of acute wounds on tumor growth depends on the predetermined wound response of the host background and its predetermined wound response.
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影响因子：
8
作者：
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通讯作者：
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影响因子：
11.2
作者：
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通讯作者：
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影响因子：
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DOI：
10.1186/bcr2780
发表时间：
2010
期刊：
Breast cancer research : BCR
影响因子：
--
作者：
Kurian AW;Fish K;Shema SJ;Clarke CA
通讯作者：
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影响因子：
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作者：
Tepper OM;Carr J;Allen RJ Jr;Chang CC;Lin CD;Tanaka R;Gupta SM;Levine JP;Saadeh PB;Warren SM
通讯作者：
Warren SM