Involvement of FoxQ1 in NSCLC through regulating EMT and increasing chemosensitivity
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Jian Feng1,*, Liqin Xu1,*, Songshi Ni1, Jun Gu1, Huijun Zhu2, Haiying Wang1, Shu Zhang2, Wei Zhang2 and Jianfei Huang2
1 Department of Respiratory Medicine, Affiliated Hospital of Nantong University. Nantong, Jiangsu, China
2 Department of Pathology, Affiliated Hospital of Nantong University. Nantong, Jiangsu, China
* These Authors contributed equally to this work
Jianfei Huang , email:
Keywords: Non-small cell lung cancer, FoxQ1, Epithelial-mesenchymal Transition, Chemosensitivity, Apoptosis
Received: April 8, 2014 Accepted: June 12, 2014 Published: June 13, 2014
Forkhead box Q1 (FoxQ1) is a member of the forkhead transcription factor family. High expression of FoxQ1 has been associated with several cancers including non-small cell lung cancer (NSCLC), but its role in the development of NSCLC is not clear. In this study, we investigated the effect of FoxQ1 up-regulated and down-regulated in vitro and in vivo, and the role of FoxQ1 in regulating epithelial-mesenchymal transition (EMT) in NSCLC, providing evidence that FoxQ1 could be a potential therapeutic target in NSCLC. NSCLC cells with silenced FoxQ1 had decreased cell proliferation, migration and invasion in cell culture and delayed growth of xenograft tumors in mice compared with corresponding control cells. The NSCLC cells downregulated for FoxQ1 induced the expression of apoptosis-associated proteins and reduction of anti-apoptotic protein expression. Downregulation of FoxQ1 promoted the expression of epithelial markers and decreased several mesenchymal markers in vitro and in vivo. In addition, FoxQ1 was associated with resistance to conventional chemotherapeutic agents. In contrast, FoxQ1 overexpressed elicited converse effects on these phenotypes in vitro and in vivo. Our findings define a key role for FoxQ1 in regulating EMT and increasing chemosensitivity in NSCLC.
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