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首页> 外文期刊>Cancer gene therapy >The glioma-associated oncogene homolog 1 promotes epithelial–mesenchymal transition in human esophageal squamous cell cancer by inhibiting E-cadherin via Snail
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The glioma-associated oncogene homolog 1 promotes epithelial–mesenchymal transition in human esophageal squamous cell cancer by inhibiting E-cadherin via Snail

机译：胶质瘤相关癌基因同源物1通过Snail抑制E-cadherin促进人食道鳞状细胞癌的上皮-间质转化

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The glioma-associated oncogene homolog 1 (GLI1) family of zinc finger transcription factors is the nuclear mediator of the Hedgehog pathway that regulates genes essential for various stages of tumor development and progression. However, the role and mechanism by which high expression of GLI1 contributes to the invasion and metastasis of human esophageal squamous cell cancer (ESCC) has not been fully elucidated. In the present study, we demonstrated that GLI1 was over-expressed in human ESCC tissues, especially in ESCC tissues with deep invasion and lymph-node metastasis. Moreover, GLI1 was also over-expressed in ESCC cell lines and correlated with the aggressiveness of ESCC cell lines. In addition, GLI signaling pathway agonist purmorphamine could increase the invasion and metastasis ability of ESCC cells in vitro. There is increasing evidence for the contribution of epithelial–mesenchymal transition (EMT) to ESCC invasion and metastasis, therefore we investigated GLI1’s role in EMT. Our results showed that high expression of GLI1 dampened expression of E-cadherin and enhanced the expression of Vimentin, and it also improved the expression of Snail, indicative of its role in EMT occurrence. Mechanistic studies showed that down-expression of Snail reversed GLI1 activation-regulated expression of EMT markers, suggesting the role of Snail in GLI1-mediated EMT. Taken together, our results had revealed that GLI1 could participate in the invasion and metastasis of ESCC through EMT. These studies indicated that in ESCC, GLI1 could be a useful target for cancer prevention and therapy.
机译：锌指转录因子的与神经胶质瘤相关的癌基因同源物1（GLI1）家族是Hedgehog途径的核介质，其调节对于肿瘤发展和进展的各个阶段必不可少的基因。但是，尚未充分阐明GLI1的高表达对人食道鳞状细胞癌（ESCC）侵袭和转移的作用和机制。在本研究中，我们证明了GLI1在人类ESCC组织中过表达，尤其是在具有深度浸润和淋巴结转移的ESCC组织中。而且，GLI1也在ESCC细胞系中过表达，并且与ESCC细胞系的侵袭性相关。此外，GLI信号通路激动剂紫吗啡胺可增加体外ESCC细胞的侵袭和转移能力。越来越多的证据表明上皮-间质转化（EMT）对ESCC侵袭和转移的贡献，因此我们研究了GLI1在EMT中的作用。我们的结果表明，GLI1的高表达抑制了E-cadherin的表达，增强了波形蛋白的表达，并且还改善了Snail的表达，表明其在EMT发生中的作用。机制研究表明Snail的下调逆转了GLI1激活的EMT标记物的表达，提示Snail在GLI1介导的EMT中的作用。两者合计，我们的结果表明，GLI1可以通过EMT参与ESCC的侵袭和转移。这些研究表明，在ESCC中，GLI1可能是预防和治疗癌症的有用靶标。

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