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FOXD1 promotes EMT and cell stemness of oral squamous cell carcinoma by transcriptional activation of SNAI2
Cell and Bioscience ( IF 7.5 ) Pub Date : 2021-08-04 , DOI: 10.1186/s13578-021-00671-9
Yang Chen 1 , Weilian Liang 1 , Ke Liu 2 , Zhengjun Shang 2
Affiliation  

Epithelial-mesenchymal transition (EMT) and cell stemness are implicated in the initiation and progression of oral squamous cell carcinoma (OSCC). Revealing the intrinsic regulatory mechanism may provide effective therapeutic targets for OSCC. In this study, we found that Forkhead box D1 (FOXD1) was upregulated in OSCC compared with normal samples. Patients with a higher FOXD1 expression had a poorer overall survival and disease-free survival. Immunohistochemical staining results showed that FOXD1 expression was related to the clinical stage and relapse status of OSCC patients. When FOXD1 expression was knocked down in CAL27 and SCC25 cells, the migration, invasion, colony formation, sphere formation, and proliferation abilities decreased. Moreover, EMT and stemness-related markers changed remarkably, which indicated that the EMT process and cell stemness were inhibited. Conversely, overexpression of FOXD1 promoted EMT and cell stemness. Further study demonstrated that FOXD1 could bind to the promoter region and activate the transcription of SNAI2. In turn, the elevated SNAI2 affected EMT and cell stemness. An in vivo study showed that FOXD1-overexpressing CAL27 cells possessed a stronger tumorigenic ability. Our findings revealed a novel mechanism in regulating EMT and cell stemness and proposed FOXD1 as a potential marker for the diagnosis and treatment of OSCC.

中文翻译:

FOXD1通过转录激活SNAI2促进口腔鳞状细胞癌的EMT和细胞干细胞

上皮间质转化 (EMT) 和细胞干细胞与口腔鳞状细胞癌 (OSCC) 的发生和进展有关。揭示内在调控机制可能为 OSCC 提供有效的治疗靶点。在这项研究中,我们发现与正常样本相比,OSCC 中 Forkhead box D1 (FOXD1) 上调。FOXD1 表达较高的患者总生存期和无病生存期较差。免疫组化染色结果显示FOXD1表达与OSCC患者的临床分期和复发状态有关。当 CAL27 和 SCC25 细胞中 FOXD1 表达被敲低时,迁移、侵袭、集落形成、球体形成和增殖能力下降。此外,EMT和干性相关标记发生了显着变化,这表明 EMT 过程和细胞干细胞受到抑制。相反,FOXD1 的过表达促进了 EMT 和细胞干性。进一步的研究表明,FOXD1 可以与启动子区域结合并激活 SNAI2 的转录。反过来,升高的 SNAI2 影响 EMT 和细胞干性。体内研究表明,过表达 FOXD1 的 CAL27 细胞具有更强的致瘤能力。我们的研究结果揭示了调节 EMT 和细胞干性的新机制,并提出 FOXD1 作为 OSCC 诊断和治疗的潜在标志物。体内研究表明,过表达 FOXD1 的 CAL27 细胞具有更强的致瘤能力。我们的研究结果揭示了调节 EMT 和细胞干性的新机制,并提出 FOXD1 作为 OSCC 诊断和治疗的潜在标志物。体内研究表明,过表达 FOXD1 的 CAL27 细胞具有更强的致瘤能力。我们的研究结果揭示了调节 EMT 和细胞干性的新机制,并提出 FOXD1 作为 OSCC 诊断和治疗的潜在标志物。
更新日期:2021-08-04
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