Pituitary tumor-transforming gene 1 (PTTG1) is overexpressed in oral squamous cell carcinoma (OSCC) and promotes migration, invasion and epithelial-mesenchymal transition (EMT) in SCC15 cells
Pituitary tumor-transforming gene 1 (PTTG1) is overexpressed in oral squamous cell carcinoma (OSCC) and promotes migration, invasion and epithelial-mesenchymal transition (EMT) in SCC15 cells
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DOI：
10.1007/s13277-014-2143-2
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发表时间：
2014-09-01
期刊：
影响因子：
--
通讯作者：
Lu, Li
中科院分区：
文献类型：
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作者：
Zhang, Enjiao;Liu, Shuang;Lu, Li
PTTG 1是一种重要的致癌转录因子，与多种恶性肿瘤有关，包括口腔鳞状细胞癌（OSCC），这是一种常见的头颈部恶性肿瘤。虽然PTTG 1在口腔鳞状细胞癌组织中过表达，但其在人类口腔鳞状细胞癌中的作用仍不明确。因此，本研究旨在探讨PTTG 1表达与口腔鳞癌发生的关系。我们首先检测了28对OSCC组织和邻近非肿瘤组织中PTTG 1 mRNA和蛋白的表达。应用免疫组化方法检测98例口腔鳞癌组织中PTTG 1蛋白的表达。我们的数据显示，PTTG 1的mRNA和蛋白表达水平在口腔鳞癌组织标本中明显高于相应的非肿瘤组织标本。PTTG 1蛋白在98例OSCC中的高表达率为75.51%（74/98），且与OSCC的淋巴结转移（P = 0.002）和TNM分期（P = 0.007）有关。此外，PTTG 1的强制过表达增强SCC 15细胞的迁移和侵袭，而PTTG 1的敲低导致相反的现象。此外，PTTG 1升高还可增加SCC 15细胞基质金属蛋白酶（MMP）-2的活性和表达，促进上皮间质转化（EMT）过程。EMT的改变伴随着上皮钙粘蛋白（E-cadherin）蛋白表达的下调和snail和波形蛋白的上调。总之，我们的研究结果表明，PTTG 1可能有助于人类口腔鳞癌的发展和进展。
Pituitary tumor-transforming gene 1 (PTTG1) is an important oncogenic transcription factor implicated in various malignancies, including oral squamous cell carcinoma (OSCC), a common malignancy of head and neck. Although PTTG1 is reportedly overexpressed in OSCC tissues, its role in human OSCC remains elusive. Thus, this study was conducted to explore the correlation between PTTG1 expression and tumorigenesis of OSCC. We first examined PTTG1 mRNA and protein expression in 28 pairs of OSCC tissues and adjacent non-tumor tissues. PTTG1 protein levels in 98 OSCC specimens were also evaluated by using immunohistochemistry. Our data showed that both mRNA and protein expression levels of PTTG1 in OSCC tissue specimens were markedly higher than that in the corresponding non-tumor tissue samples. A high level of PTTG1 protein expression was found in 74 out of 98 cases (75.51 %) and it was correlated with lymph node metastasis (P = 0.002) and tumor-node-metastasis (TNM) stage (P = 0.007) of patients with OSCC. Moreover, forced overexpression of PTTG1 enhanced SCC15 cell migration and invasion, whereas knockdown of PTTG1 resulted in reverse phenomena. In addition, elevated PTTG1 also increased the activities and expressions of matrix metalloproteinase (MMP)-2, and enhanced epithelial-mesenchymal-transition (EMT) process in SCC15 cells. The EMT changes were accompanied by downregulation of epithelial cadherin (E-cadherin) protein expression and upregulation of snail and vimentin. In summary, our results illustrate that PTTG1 may contribute to the development and progression of human OSCC.