A study on epithelial-mesenchymal transition mediated by deltaNp63 in invasion and metastasis of oral squamous cell carcinoma

在这项研究中，我们研究了deltaNp 63在口腔鳞状细胞癌（OSCC）进展过程中EMT的作用。在OSCC细胞中检测到deltaNp 63和上皮标志物的表达，但在SQUU-B细胞（高转移潜能）中未检测到。间充质标志物在SQUU-B细胞中强烈表达。敲低内源性deltaNp 63可诱导HSC-2细胞形态学改变为梭形，上皮标志物表达减少，间充质标志物表达增加，迁移增加。相反，过表达deltaNp 63的SQUU-B细胞显示其形态从基质细胞样改变为上皮细胞。免疫组化染色显示deltaNp 63表达强度降低与口腔鳞癌患者的转移和不良预后呈正相关。这些结果表明，癌细胞中的deltaNp 63下调诱导与OSCC的肿瘤进展相关的间充质表型。

In this study, we investigated the role of deltaNp63 in EMT during progression of oral squamous cell carcinoma (OSCC). The expressions of deltaNp63 and epithelial markers was detected in the OSCC cells, but not in SQUU-B cells (high metastatic potential). Mesenchymal markers were strongly expressed in the SQUU-B cells. Knockdown of endogenous deltaNp63 in HSC-2 cells induced morphological changes to the spindle shape, decreased the expression of epithelial markers, increased the expression of mesenchymal markers, increased migration. By contrast, SQUU-B cells overexpressing deltaNp63 showed changed their morphology from stromal cell-like to epithelial cells. Immunohistochemical staining revealed decreased intensity of deltaNp63 was positively associated with metastases and poor prognosis in the OSCC patients. These results indicated that deltaNp63 downregulation in cancer cells induces a mesenchymal phenotype that is related to tumor progression of OSCC.