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- W2569015585 abstract "Osteopontin (secreted phosphoprotein 1; SPP1) expression has been identified in human lung cancer and has been linked with enhanced tumour progression. To examine its functional role, we induced lung tumours by repetitive urethane or MCA/BHT lung carcinogens in C57BL/6 mice lacking both (<i>Spp1-/-</i>), one (<i>Spp1+/-</i>), or no (<i>Spp1+/+</i>) copy of the endogenous <i>Spp1</i> gene. Primary end-points were lung tumour number and size; secondary end-points were SPP1 expression, epithelial cell survival, carcinogen-induced inflammation, and angiogenesis. Data are presented as mean ± SD. Compared with <i>Spp1+/+</i> mice (n = 22), <i>Spp1-/-</i> mice (n = 25) developed dramatically fewer and significantly smaller lung tumours in response to urethane, while <i>Spp1±</i> mice (n = 12) behaved similar to <i>Spp1-/-</i> mice (number/diameter of lung tumours in <i>Spp1+/+</i>, <i>Spp1+/-</i>, and <i>Spp1-/-</i> mice, respectively: 16.1 ± 12.7/1.2 ± 0.3 mm, 2.4 ± 2.3/0.9 ± 0.2 mm, and 1.3 ± 1.6/0.7 ± 0.2 mm; P < 0.05 for comparison of <i>Spp1+/+</i> with <i>Spp1-/-</i> and <i>Spp1+/-</i> mice). <i>Spp1-/-</i> mice were also protected from two-hit MCA/BHT-oncogenesis compared with <i>Spp1+/+</i> controls. <i>Spp1-/-</i> mice displayed decreased epithelial cell survival and reduced numbers of airspace macrophages early after urethane, and enhanced tumour cell apoptosis and limited tumour angiogenesis at late stages of lung tumour progression. SPP1 was expressed in the naïve lung by non-ciliated airway epithelial cells and alveolar macrophages and was significantly up-regulated during multi-stage lung carcinogenesis. Our data indicate that SPP1 is functionally involved in airway epithelial carcinogenesis and may present a target for lung cancer treatment and prevention." @default.
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- W2569015585 date "2016-11-15" @default.
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- W2569015585 title "S8 Osteopontin as an airway epithelial tumour promoter" @default.
- W2569015585 doi "https://doi.org/10.1136/thoraxjnl-2016-209333.14" @default.
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