4.4 Article

CD147 promotes proliferation and migration of oral cancer cells by inhibiting junctions between E-cadherin and β-catenin

期刊

JOURNAL OF ORAL PATHOLOGY & MEDICINE
卷 49, 期 10, 页码 1019-1029

出版社

WILEY
DOI: 10.1111/jop.13088

关键词

CD147; BSG; E-cadherin; epithelial-mesenchymal transition; migration; oral squamous cell carcinoma

资金

  1. National Natural Science Foundation of China [81873717]
  2. Natural Science Foundation of Hunan Province [2017JJ2392, 2019JJ40508]

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Background Although association between oral squamous cell carcinoma (OSCC) with epithelial-mesenchymal transition (EMT) has been demonstrated, we found CD147, one transmembrane protein we previously studied in oral submucous fibrosis, was correlated with E-cadherin, one marker of EMT. Here, we investigated CD147 expression in the different stages of OSCC and assessed its association with epithelial-mesenchymal transition (EMT). Materials and methods CD147 and E-cadherin expression in tissue microarrays containing 48 OSCC specimens and matched adjacent tissues was analysed using immunohistochemistry. CD147 was overexpressed or knocked down using exogenous cloning vector and RNA interference, respectively, in OSCC cell lines. Cell proliferation and migration were measured using the CCK8 assay and scratch test, respectively. The expression and localization of EMT-associated proteins was analysed by Western blotting and immunofluorescence. Results CD147 expression in OSCC tissues was significantly higher than that in adjacent tissues and was markedly higher in cancer tissues with metastasis (P < .05). CD147 expression showed significant negative correlation with E-cadherin expression. CD147 overexpression downregulated E-cadherin and inhibited its complex with beta-catenin and then upregulated N-cadherin and vimentin. Additionally, alterations in CD147 protein expression affected proliferation and migration ability in OSCC cells and were related to beta-catenin nuclear translocation. Conclusion CD147 plays an important role in tumorigenesis and metastasis by promoting EMT progression in OSCC. It may be considered as a novel potential diagnostic and therapeutic target for OSCC.

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