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

Abstract

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 β‐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 β‐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.

Drug Delivery (Nano)Platforms for Oral and Dental Applications: Tissue Regeneration, Infection Control, and Cancer Management

“…A variety of molecular pathways accounting for oral cancer malignancy have been identified. Metastasis of oral cancer cells is mediated via upregulation of epithelial‐to‐mesenchymal transition, [ 268 ] matrix metalloproteinases, [ 269 ] microRNAs, [ 270 ] and long non‐coding RNAs. [ 271 ] In addition, PI3K/Akt/mTOR, [ 272 ] Wnt, [ 273 ] STAT3, [ 274 ] and TGF‐ β [ 275 ] contribute to oral cancer proliferation.…”

Type 2 diabetes mellitus promotes the proliferation, metastasis, and suppresses the apoptosis in oral squamous cell carcinoma

“…Photomicrographs were captured at time points of 0, 12, and 24 hours under DMI3000 B microscope system (Leica, Germany). The closed wound areas were measured by Image J software as previously introduced 13 …”

“…The closed wound areas were measured by Image J software as previously introduced. 13 Annexin V-FITC+and 7-AAD-staining was identified as early apoptotic cells while Annexin V-FITC+and 7-AAD+staining symbolized late apoptotic cells.…”

Epithelial–Mesenchymal Transition Associated with Head and Neck Squamous Cell Carcinomas: A Review

“…E-cadherin is considered the main marker of the EMT phenomenon and may be the main molecule that is impaired. E-cadherin reduction leads to several alterations, such as a loss of intercellular adhesion, alterations of the basal membrane, and the induction of the nuclear translocation of β-catenin [ 31 ]. E-cadherin promotes the formation of calcium-dependent cell–cell adhesion through homophylic interactions between two molecules of cadherin on the cell surface and stabilizes adhesive attachments.…”