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Year : 2016  |  Volume : 53  |  Issue : 1  |  Page : 20-24

P120ctn may participate in epithelial-mesenchymal transition in OSCC

1 Chongqing Key Laboratory for Oral Diseases and Biomedical Sciences, Stomatology Hospital of Chongqing Medical University, Chongqing, China
2 State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, China
3 Department of Stomatology, Xiamen Medical College, Xiamen, China

Correspondence Address:
D Feng
Chongqing Key Laboratory for Oral Diseases and Biomedical Sciences, Stomatology Hospital of Chongqing Medical University, Chongqing
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0019-509X.180821

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Aim: Oral squamous cell carcinoma (OSCC) is the eighth most common cause of cancer death. OSCC cells can easily invade tissues and metastasize to the cervical lymph nodes. Understanding the molecular basis of OSCC metastasis would facilitate the development of new therapeutic approaches to the disease. Materials and Methods: To identify the potential role of catenin (P120ctn) in the progression of OSCC, HN4 cells (derived from a primary OSCC) and HN12 cells (derived from a lymph node metastasis in the same patient) were used in the present study. The samples of 28 patients with OSCC were examined to determine the expression of P120ctn and E-cadherin (E-cad; E: Epithelial) in vivo. Then, P120ctn was subsequently knocked down in HN4 cells (HN4/shP120ctn) and overexpressed in HN12 cells (HN12/P120ctn). Invasion and migration capacity, as well as the expression of the epithelial-to-mesenchymal transition (EMT) markers N-cadherin and vimentin were detected. Results: The results showed a positive correlation between the expression of P120ctn and E-cad in OSCC samples. The overexpression of P120ctn led to a decrease in both invasion and migration capacity of HN12 cells accompanied by a decrease in EMT markers. In contrast, knockdown of P120ctn led to an increase in both invasion and migration capacity accompanied by an increase in EMT markers. Conclusion: Considered together, we concluded that P120ctn might regulate EMT in OSCC through E-cad. The proper expression of P120ctn might therefore serve as a therapeutic goal for the inhibition of OSCC progression.


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