Oncotarget

Research Papers:

Flotillin-2 promotes nasopharyngeal carcinoma metastasis and is necessary for the epithelial-mesenchymal transition induced by transforming growth factor-β

Liang Zhao, Li Lin, Changqie Pan, Min Shi, Yulin Liao, Jianping Bin and Wangjun Liao _

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Oncotarget. 2015; 6:9781-9793. https://doi.org/10.18632/oncotarget.3382

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Abstract

Liang Zhao1*, Li Lin1*, Changqie Pan1, Min Shi1, Yulin Liao2, Jianping Bin2, Wangjun Liao1

1Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou Guangdong 510515, China

2Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou Guangdong 510515, China

*These authors have contributed equally to this work

Correspondence to:

Wangjun Liao, e-mail: [email protected]

Keywords: nasopharyngeal carcinoma, Flotillin-2, transforming growth factor-β, epithelial-mesenchymal transition, metastasis

Received: January 15, 2015     Accepted: February 14, 2015     Published: April 07, 2015

ABSTRACT

Transforming growth factor-β (TGF-β) promotes cancer metastasis via the epithelial-mesenchymal transition (EMT) but the underlying mechanisms in nasopharyngeal carcinoma (NPC) remain unclear. Flotillin-2 (Flot2), a specialized lipid raft domain in cellular membrane, was reported to promote cancer metastasis. Recently, in neuropathy, it was also suggested that Flot2 was involved in Src activation, which is known as the downstream signal of TGF-β. Therefore, we intended to find out the relationship between Flot2 and TGF-β in the process of nasopharyngeal carcinoma (NPC) metastasis. In this study, we found that Flot2 expression level positively correlated with the cancer stage in NPC tissues. Elevated Flot2 in tumor tissue was an independent prognostic marker, and higher Flot2 expression level showed shorter overall survival time in 181 NPC patients. In NPC cells, silencing Flot2 reversed the metastatic effect induced by TGF-β. Moreover, TGF-β-induced Src phosphorylation was significantly inhibited by Flot2 knocking down. As the consequence of Flot2 inhibition, the expression of the epithelial biomarker E-cadherin was upregulated, while the mesenchymal marker vimentin and signaling transducer β-catenin was suppressed. In conclusions, Flot2 is an indispensable member for TGF-β signaling, which is essential for the EMT process in NPC metastasis. Suppressing Flot2 may be a novel way against TGF-β-induced EMT.


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