Peroxiredoxin 1 promotes invasion and migration by regulating epithelial-to-mesenchymal transition during oral carcinogenesis.
Peroxiredoxin 1 promotes invasion and migration by regulating epithelial-to-mesenchymal transition during oral carcinogenesis.
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过氧化还原蛋白 1 通过调节口腔癌发生过程中的上皮间质转化来促进侵袭和迁移
DOI:
10.18632/oncotarget.9705
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发表时间:
2016-07-26
期刊:
影响因子:
--
通讯作者:
Tang X
中科院分区:
文献类型:
--
作者:
Niu W;Zhang M;Chen H;Wang C;Shi N;Jing X;Ge L;Chen T;Tang X
Tobacco smoking is the major risk factor for oral squamous cell carcinoma (OSCC). Previously, we found that nicotine up-regulates peroxiredoxin 1 (Prx1), an important antioxidant enzyme, and nuclear factor kappa B (NFκB) in OSCC cells. However, the molecular mechanism of Prx1 in oral carcinogenesis remains obscure. To improve our understanding of the functional role of Prx1 during the cascade of tobacco-associated oral carcinogenesis, we characterized Prx1, NFκB, and epithelial-to-mesenchymal transition (EMT) markers including E-cadherin, vimentin and Snail in 30 primary oral tumors (15 from smokers with OSCC and 15 from non-smokers with OSCC) and 10 normal oral mucosa specimens from healthy individuals. The expression levels of Prx1, nuclear NFκB, vimentin and Snail were higher in the tumors from smokers with OSCC than in those from non-smokers with OSCC or the healthy controls. The expression levels of E-cadherin showed an opposite trend. Prx1 silencing suppressed the nicotine-induced EMT, cell invasion and migration in SCC15 cells in vitro. Furthermore, Prx1 activated the NFκB pathway in SCC15 cells. Prx1 might therefore play an oncogenic role in tobacco-related OSCC and thus serve as a target for chemopreventive and therapeutic interventions.
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DOI:
10.1002/hed.10004
发表时间:
2002-02-01
影响因子:
2.9
作者:
Funk, GF;Karnell, LH;Hoffman, HT
通讯作者:
Hoffman, HT
影响因子:
6.4
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Chellappan, Srikumar
影响因子:
2.6
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通讯作者:
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影响因子:
11.2
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影响因子:
4.8
作者:
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通讯作者:
Pan, Quintin