PDF(Pubmed)
Abstract：
BACKGROUND: Epithelial-mesenchymal transition (EMT) enables tumor cell invasion and metastasis. Many studies have demonstrated the critical role of EMT in lymph node metastasis in oral squamous cell carcinoma (OSCC). During EMT, epithelial cancer cells lose intercellular adhesion and apical-basal polarity and acquire mesenchymal properties such as motility and invasiveness. A significant feature of EMT is cadherin switching, involving the downregulation of E-cadherin and upregulation of N-cadherin. The TGF-β/SMAD pathway can also induce EMT. We aimed to evaluate EMT markers as predictors of lymph node metastasis in OSCC.
METHODS: We performed genetic profiling of 159 primary OSCCs from TCGA and analyzed the expression of EMT markers, including cadherin switch genes (CDH1, CDH2), and TGF-β/SMAD pathway genes. Samples were divided into advanced (stage III-IV) and early (stage I-II) stage groups. Differential expression analysis was performed, as well as an independent validation study containing fresh OSCC samples.
RESULTS: TGF-β/SMAD pathway genes such as SMAD6 were upregulated in advanced stage tumors. N-cadherin and SNAIL2 were overexpressed in node-positive tumors. Keratins were downregulated in these groups.
CONCLUSIONS: Our findings demonstrate that EMT marker expression correlates with lymph node metastasis in OSCC. Developing therapies targeting regulators such as N-cadherin may prevent metastasis and improve outcomes.
METHODS: We performed genetic profiling of 159 primary OSCCs from TCGA and analyzed the expression of EMT markers, including cadherin switch genes (CDH1, CDH2), and TGF-β/SMAD pathway genes. Samples were divided into advanced (stage III-IV) and early (stage I-II) stage groups. Differential expression analysis was performed, as well as an independent validation study containing fresh OSCC samples.
RESULTS: TGF-β/SMAD pathway genes such as SMAD6 were upregulated in advanced stage tumors. N-cadherin and SNAIL2 were overexpressed in node-positive tumors. Keratins were downregulated in these groups.
CONCLUSIONS: Our findings demonstrate that EMT marker expression correlates with lymph node metastasis in OSCC. Developing therapies targeting regulators such as N-cadherin may prevent metastasis and improve outcomes.
摘要：
背景：上皮-间质转化（EMT）能够促进肿瘤细胞的侵袭和转移。许多研究表明EMT在口腔鳞状细胞癌（OSCC）淋巴结转移中的关键作用。EMT期间,上皮性癌细胞失去细胞间粘附和顶端-基底极性，并获得间充质特性，如运动性和侵袭性。EMT的一个显著特征是钙粘蛋白的转换，涉及E-cadherin的下调和N-cadherin的上调。TGF-β/SMAD途径也可诱导EMT。我们旨在评估EMT标志物作为OSCC淋巴结转移的预测因子。
方法：我们对来自TCGA的159个原发性OSCC进行了遗传分析，并分析了EMT标记的表达，包括钙粘蛋白开关基因(CDH1，CDH2)，和TGF-β/SMAD通路基因。将样品分为晚期(III-IV期)和早期(I-II期)阶段组。进行差异表达分析，以及包含新鲜OSCC样本的独立验证研究。
结果：TGF-β/SMAD通路基因如SMAD6在晚期肿瘤中上调。N-cadherin和SNAIL2在淋巴结阳性肿瘤中过表达。角蛋白在这些组中下调。
结论：我们的研究结果表明，在OSCC中，EMT标志物的表达与淋巴结转移相关。开发靶向调节因子如N-钙粘蛋白的疗法可以预防转移并改善结果。
方法：我们对来自TCGA的159个原发性OSCC进行了遗传分析，并分析了EMT标记的表达，包括钙粘蛋白开关基因(CDH1，CDH2)，和TGF-β/SMAD通路基因。将样品分为晚期(III-IV期)和早期(I-II期)阶段组。进行差异表达分析，以及包含新鲜OSCC样本的独立验证研究。
结果：TGF-β/SMAD通路基因如SMAD6在晚期肿瘤中上调。N-cadherin和SNAIL2在淋巴结阳性肿瘤中过表达。角蛋白在这些组中下调。
结论：我们的研究结果表明，在OSCC中，EMT标志物的表达与淋巴结转移相关。开发靶向调节因子如N-钙粘蛋白的疗法可以预防转移并改善结果。
