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首页> 外文期刊>Tumour biology : >Interaction with CCNH/CDK7 facilitates CtBP2 promoting esophageal squamous cell carcinoma (ESCC) metastasis via upregulating epithelial-mesenchymal transition (EMT) progression
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Interaction with CCNH/CDK7 facilitates CtBP2 promoting esophageal squamous cell carcinoma (ESCC) metastasis via upregulating epithelial-mesenchymal transition (EMT) progression

机译：与CCNH / CDK7的相互作用可通过上调上皮-间质转化（EMT）进程促进CtBP2促进食管鳞状细胞癌（ESCC）转移

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摘要

CtBP2, as a transcriptional corepressor of epithelial-specific genes, has been reported to promote tumor due to upregulating epithelial-mesenchymal transition (EMT) in cancer cells. CtBP2 was also demonstrated to contribute to the proliferation of esophageal squamous cell carcinoma (ESCC) cells through a negative transcriptional regulation of p16(INK4A). In this study, for the first time, we reported that CtBP2 expression, along with CCNH/CDK7, was higher in ESCC tissues with lymph node metastases than in those without lymph node metastases. Moreover, both CtBP2 and CCNH/CDK7 were positively correlated with E-cadherin, tumor grade, and tumor metastasis. However, the concrete mechanism of CtBP2's role in enhancing ESCC migration remains incompletely understood. We confirmed that CCNH/CDK7 could directly interact with CtBP2 in ESCC cells in vivo and in vitro. Furthermore, our data demonstrate for the first time that CtBP2 enhanced the migration of ESCC cells in a CCNH/CDK7-dependent manner. Our results indicated that CCNH/CDK7-CtBP2 axis may augment ESCC cell migration, and targeting the interaction of both may provide a novel therapeutic target of ESCC.
机译：据报道，CtBP2作为上皮特异性基因的转录共表达抑制剂，由于上调了癌细胞中的上皮-间质转化（EMT）而促进了肿瘤的发展。还证实了CtBP2通过对p16（INK4A）的负转录调节来促进食管鳞状细胞癌（ESCC）细胞的增殖。在本研究中，我们首次报道在有淋巴结转移的ESCC组织中，CtBP2表达以及CCNH / CDK7高于无淋巴结转移的ESCC组织。此外，CtBP2和CCNH / CDK7均与E-钙粘蛋白，肿瘤等级和肿瘤转移呈正相关。但是，CtBP2在增强ESCC迁移中作用的具体机制仍未完全了解。我们证实CCNH / CDK7可以在体内和体外直接与ESCC细胞中的CtBP2相互作用。此外，我们的数据首次证明CtBP2以CCNH / CDK7依赖性方式增强了ESCC细胞的迁移。我们的研究结果表明CCNH / CDK7-CtBP2轴可能会增加ESCC细胞的迁移，并且靶向两者的相互作用可能会提供ESCC的新型治疗靶点。

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