共 32 条
Prolonged Nitric Oxide Exposure Enhances Anoikis Resistance and Migration through Epithelial-Mesenchymal Transition and Caveolin-1 Upregulation
被引:21
作者:

Chanvorachote, Pithi
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h-index: 0
机构:
Chulalongkorn Univ, Fac Pharmaceut Sci, Dept Physiol & Pharmacol, Bangkok 10330, Thailand Chulalongkorn Univ, Fac Pharmaceut Sci, Dept Physiol & Pharmacol, Bangkok 10330, Thailand

Pongrakhananon, Varisa
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h-index: 0
机构: Chulalongkorn Univ, Fac Pharmaceut Sci, Dept Physiol & Pharmacol, Bangkok 10330, Thailand

Chunhacha, Preedakorn
论文数: 0 引用数: 0
h-index: 0
机构: Chulalongkorn Univ, Fac Pharmaceut Sci, Dept Physiol & Pharmacol, Bangkok 10330, Thailand
机构:
[1] Chulalongkorn Univ, Fac Pharmaceut Sci, Dept Physiol & Pharmacol, Bangkok 10330, Thailand
关键词:
POOR-PROGNOSIS;
CELL-MIGRATION;
METASTASIS;
EXPRESSION;
APOPTOSIS;
INHIBITION;
INVASION;
SURVIVAL;
GROWTH;
EMT;
D O I:
10.1155/2014/941359
中图分类号:
Q81 [生物工程学(生物技术)];
Q93 [微生物学];
学科分类号:
071005 ;
0836 ;
090102 ;
100705 ;
摘要:
Nitric oxide (NO) in tumor microenvironment may have a significant impact on metastatic behaviors of cancer. Noncytotoxic doses of NO enhanced anoikis resistance and migration in lung cancer H23 cells via an increase in lamellipodia, epithelial-mesenchymal transition (EMT) markers including vimentin and snail, and caveolin-1 (Cav-1). However, the induction of EMT was found in Cav-1-knock down cells treated with NO, suggesting that EMT was through Cav-1-independent pathway. These effects of NO were consistently observed in other lung cancer cells including H292 and H460 cells. These findings highlight the novel role of NO on EMT and metastatic behaviors of cancer cells.
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