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首页> 外文期刊>Cell biology international. >Nf-kbp65 promotes invasion and metastasis of oesophageal squamous cell cancer by regulating matrix metalloproteinase-9 and epithelial-to-mesenchymal transition
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Nf-kbp65 promotes invasion and metastasis of oesophageal squamous cell cancer by regulating matrix metalloproteinase-9 and epithelial-to-mesenchymal transition

机译：Nf-kbp65通过调节基质金属蛋白酶9和上皮-间质转化促进食管鳞状细胞癌的侵袭和转移

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摘要

NF-kB has been recognized as one of the factors responsible for the development of cancer; however, the mechanism by which high expression of NF-kB contributes to the progression of human oesophageal squamous cell cancer (ESCC) is not fully understood. In our investigations, NF-kBP65 was overexpressed in human ESCC tissues, especially in ESCC tissues with deep invasion and lymph node metastasis. Suppression of NF-kBP65 by siRNA decreased the invasion and proliferation ability of EC9706 cells in vitro. Furthermore, siRNA-mediated NF-kBP65 knock-down could lead to the downregulation of MMP-9, a metastasis-related gene. Reduced E-cadherin is a hallmark of invasive carcinomas that have acquired mesenchymal-epithelial transition (EMT) phenotypes and Vimentin is another molecule that is used widely as a marker of the EMT. We found upregulation of E-cadherin expression and downregulation of Vimentin was induced by NF-kBP65 siRNA, which suggests that NF-kBP65 siRNAcould inhibit the invasion and proliferation ability of ECSS through attenuating the expression ofMMP-9 and EMT. Thus, ESCC NF-kBP65 could be a useful target for cancer prevention and therapy.
机译：NF-kB已被认为是导致癌症发展的因素之一。但是，尚不清楚NF-κB的高表达促进人食道鳞状细胞癌（ESCC）进展的机制。在我们的研究中，NF-kBP65在人类ESCC组织中，特别是在具有深浸润和淋巴结转移的ESCC组织中过表达。 siRNA抑制NF-kBP65可降低EC9706细胞的体外侵袭和增殖能力。此外，siRNA介导的NF-kBP65敲低可能导致MMP-9（与转移相关的基因）下调。降低的E-钙黏着蛋白是已获得间充质-上皮转化（EMT）表型的浸润性癌的标志，而波形蛋白（Vimentin）是另一种广泛用作EMT标记物的分子。我们发现NF-kBP65 siRNA诱导了E-钙黏着蛋白表达的上调和波形蛋白的下调，这表明NF-kBP65 siRNA可以通过减弱MMP-9和EMT的表达来抑制ECSS的侵袭和增殖能力。因此，ESCC NF-kBP65可能是预防和治疗癌症的有用靶标。

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