Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
Department of Medical Research, Chung Shan Medical University Hospital, Taichung 402, Taiwan.
Cells. 2020 Mar 13;9(3):704. doi: 10.3390/cells9030704.
Epithelial-mesenchymal transition (EMT) is strongly correlated with tumor metastasis and contains several protein markers, such as E-cadherin. Carbonic anhydrase III (CA III) exhibits low carbon dioxide hydratase activity in cancer. However, the detailed mechanisms of CA III and their roles in oral cancer are still unknown. This study established a CA III-overexpressed stable clone and observed the expression of CA III protein in human SCC-9 and SAS oral cancer cell lines. The migration and invasion abilities were determined using a Boyden chamber assay. Our results showed that the overexpression of CA III protein significantly increased the migration and invasion abilities in oral cancer cells. Moreover, a whole genome array analysis revealed that CA III regulated epithelial-mesenchymal transition by reducing the expression of epithelial markers. Data from the GEO database also demonstrated that CA III mRNA is negatively correlated with CDH1 mRNA. Mechanistically, CA III increased the cell motility of oral cancer cells through the FAK/Src signaling pathway. In conclusion, this suggests that CA III promotes EMT and cell migration and is potentially related to the FAK/Src signaling pathway in oral cancer.
上皮-间充质转化 (EMT) 与肿瘤转移密切相关，包含几个蛋白标志物，如 E-钙黏蛋白。碳酸酐酶 III (CA III) 在癌症中表现出低二氧化碳水合酶活性。然而，CA III 的详细机制及其在口腔癌中的作用仍不清楚。本研究建立了 CA III 过表达稳定克隆，并观察 CA III 蛋白在人 SCC-9 和 SAS 口腔癌细胞系中的表达。使用 Boyden 室测定法确定迁移和侵袭能力。我们的结果表明，CA III 蛋白的过表达显著增加了口腔癌细胞的迁移和侵袭能力。此外，全基因组阵列分析表明，CA III 通过降低上皮标志物的表达来调节上皮-间充质转化。GEO 数据库的数据还表明，CA III mRNA 与 CDH1 mRNA 呈负相关。从机制上讲，CA III 通过 FAK/Src 信号通路增加口腔癌细胞的细胞迁移能力。总之，这表明 CA III 促进 EMT 和细胞迁移，并可能与口腔癌中的 FAK/Src 信号通路有关。
