Abstract
 
Vol 48 No. 3: 229-237 [PDF] [Full Text]
 
β-Catenin is important for cancer stem cell generation and tumorigenic activity in nasopharyngeal carcinoma
 
Rui Jiang, Xiaoshuang Niu, Yuxiang Huang and Xiaosheng Wang*
 
Department of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai 2000031, China
 

Abstract  Nasopharyngeal carcinoma (NPC) is one of the most common malignant tumors with poor prognosis and recurrence in South China. The hard eradication of NPC in clinic is predominantly due to cancer stem cells (CSCs). Increasing evidence revealed that the aberrant activation of Wnt/β-catenin was positively correlated with the produce of CSCs. To further investigate the effect of β-catenin on CSCs and tumorigenesis in NPC, a CNE2 cell line (pLKO.1-sh-β-catenin-CNE2) with stably suppressed expression of β-catenin was used in this study. The expressions of biomarkers in CSCs including c-myc, Nanog, Oct3/4, Sox2, EpCAM as well as adhesion-related proteins like E-cadherin and vimentin were analyzed by western blot analysis and immunofluorescent staining. The proliferation and migration abilities were investigated by MTT assay and Transwell assay, respectively. Cell cycle was analyzed by flow cytometry. Finally, xenograft was performed to determine the effect of β-catenin on oncogenesis in vivo. Results showed that the expressions of c-myc, Nanog, Oct3/4, Sox2, and EpCAM were all decreased in pLKO.1-sh-β-catenin-CNE2 cells. It was also found that vimentin was downregulated, while E-cadherin was upregulated. Results of MTT and Transwell assays suggested that the proliferation and migration abilities were impaired by silencing of β-catenin, and more cells were arrested in G1 phase when compared with the control. In vivo study indicated that the tumor growth was markedly suppressed in experimental group. Based on current findings, β-catenin may function as an essential protein for the maintenance of migration and proliferation abilities of NPC cells, and a complicated network consisting of c-myc, Nanog, Oct3/4, Sox2, EpCAM, E-cadherin, vimentin, and β-catenin may be involved in the inherent regulation mechanisms.

 

Keywords   CNE2 cell line; cancer stem cell; β-catenin; tumorigenic capability

 

Received   2015-10-12  
Accepted  
2015-11-28

 

Funding  This work was supported by a grant from the Shanghai Committee of Science and Technology (No. 124119a6202).

 

* Correspondence address  Tel: +86-21-64175590; Fax: +86-21-64174774; E-mail: [email protected]

 
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