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Abstract
Formin-like 3 (FMNL3) plays a crucial role in cytoskeletal mediation and is potentially a biomarker for cell migration; however, its role in cancer metastasis remains unknown. In this study, we found elevated FMNL3 protein expression in clinical nasopharyngeal carcinoma (NPC) tissues. FMNL3 expression positively correlated to the clinical stage, T (tumour), N (lymph node metastasis) and M (distant metastasis) classification of NPC patients. Moreover, FMNL3 positively correlated to Vimentin expression and negatively correlated to E-cadherin expression in clinical NPC samples. In vitro experiments showed that FMNL3 expression was inversely related to NPC cell differentiation status. Overexpression of FMNL3 led to epithelial-to-mesenchymal transition (EMT) in well differentiated CNE1 cells. TGF-β1-treated poorly differentiated CNE2 cells showed changes in EMT accompanied by enhanced FMNL3 expression and cell migration. On the contrary, knockdown of FMNL3 partially attenuated the TGF-β1-promoted CNE2 cell migration, together with associated changes in EMT markers. Finally, knockdown of FMNL3 also weakened EMT in tumours in xenographs. Our study indicates for the first time that TGF-β1/FMNL3 signalling may be a novel mechanism mediating EMT in NPC, which is closely associated with NPC metastasis.
Highlights
Formin-like 3 (FMNL3) plays a crucial role in cytoskeletal mediation and is potentially a biomarker for cell migration; its role in cancer metastasis remains unknown
Our study indicates for the first time that TGF-β1/FMNL3 signalling may be a novel mechanism mediating epithelial-to-mesenchymal transition (EMT) in Nasopharyngeal carcinoma (NPC), which is closely associated with NPC metastasis
We previously found that inhibition of PI3K/Akt signalling significantly reverses the process of EMT in NPC cells, thereby repressing the pulmonary metastasis of tumour cell-bearing nude nice[11], which highlights the clinical application of targeting EMT in NPC
Summary
Formin-like 3 (FMNL3) plays a crucial role in cytoskeletal mediation and is potentially a biomarker for cell migration; its role in cancer metastasis remains unknown. FMNL3 expression positively correlated to the clinical stage, T (tumour), N (lymph node metastasis) and M (distant metastasis) classification of NPC patients. TGF-β1-treated poorly differentiated CNE2 cells showed changes in EMT accompanied by enhanced FMNL3 expression and cell migration. Knockdown of FMNL3 partially attenuated the TGF-β1-promoted CNE2 cell migration, together with associated changes in EMT markers. Our study indicates for the first time that TGF-β1/FMNL3 signalling may be a novel mechanism mediating EMT in NPC, which is closely associated with NPC metastasis. There are major three clinical features of NPC: (1) low grade differentiation; the majority of the histological types are non-keratinizing undifferentiated carcinoma with 100% Epstein-Barr virus (EBV) infection; (2) early metastasis; nearly 60% of NPC patients suffer from local lymph node metastasis at first diagnosis; and (3) sensitivity to radiation therapy, but with a high recurrence rate. Correspondence and requests for materials should be addressed to W.J
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