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首页> 外文期刊>Cellular Physiology and Biochemistry >Krüppel-Like Factor 4 Inhibits Pancreatic Cancer Epithelial-to-Mesenchymal Transition and Metastasis by Down-Regulating Caveolin-1 Expression
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Krüppel-Like Factor 4 Inhibits Pancreatic Cancer Epithelial-to-Mesenchymal Transition and Metastasis by Down-Regulating Caveolin-1 Expression

机译：Krüppel样因子4通过下调Caveolin-1的表达抑制胰腺癌上皮-间充质转化和转移。

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Background/Aims Krüppel-like factor 4 (KLF4), a member of the KLF family of zinc finger transcription factors, has been identified as a tumor suppressor gene in a variety of tumors. However, the molecular mechanisms by which KLF4 inhibits epithelial-to-mesenchymal transition (EMT) and metastasis in pancreatic cancer remain unclear. Methods KLF4 expression in pancreatic cancer was analyzed using public datasets (Oncomine and The Cancer Genome Atlas). The expression of KLF4, caveolin-1 (Cav-1), E-cadherin, and vimentin, and their correlations with clinicopathological characteristics were evaluated by immunohistochemistry in pancreatic cancer tissues. The biological functions and underlying mechanisms of KLF4 expression on EMT and metastasis were also investigated in vitro and in vivo. Results Public datasets showed that KLF4 expression was significantly decreased in pancreatic cancer and correlated with the depth of invasion and disease stage. The expression of KLF4, Cav-1, E-cadherin, and vimentin protein in pancreatic cancer tissues was closely associated with pathological grade, disease stage, and metastasis. KLF4 expression was also positively correlated with E-cadherin expression and negatively correlated with vimentin expression, whereas Cav-1 expression was negatively associated with E-cadherin expression and positively correlated with vimentin expression. Knockdown of KLF4 expression promoted EMT and facilitated pancreatic cancer cell growth and metastasis in vitro and in vivo. In addition, immunohistochemistry (IHC) results indicated that KLF4 expression was negatively correlated with Cav-1 expression. Furthermore, down-regulating KLF4 expression increased Cav-1 and vimentin expression and decreased E-cadherin expression. Mechanistically, KLF4 could transcriptionally inhibit Cav-1 expression by binding directly to the promoter domain of Cav-1. Conclusions KLF4 inhibits pancreatic cancer EMT and metastasis by down-regulating Cav-1 expression, suggesting that the KLF4/Cav-1 signaling pathway may be a novel diagnostic and therapeutic target.
机译：背景/目的Krüppel样因子4（KLF4）是锌指转录因子KLF家族的成员，已被鉴定为多种肿瘤的抑癌基因。然而，KLF4抑制胰腺癌上皮-间质转化（EMT）和转移的分子机制仍不清楚。方法使用公开数据集（Oncomine和The Cancer Genome Atlas）分析胰腺癌中KLF4的表达。免疫组织化学方法检测胰腺癌组织中KLF4，caveolin-1（Cav-1），E-cadherin和波形蛋白的表达及其与临床病理特征的相关性。还在体外和体内研究了KLF4表达对EMT和转移的生物学功能和潜在机制。结果公开数据显示胰腺癌中KLF4表达显着降低，且与浸润深度和疾病分期有关。胰腺癌组织中KLF4，Cav-1，E-cadherin和波形蛋白的表达与病理分级，疾病分期和转移密切相关。 KLF4表达也与E-钙粘蛋白表达呈正相关，与波形蛋白表达呈负相关，而Cav-1表达与钙粘蛋白表达呈负相关，与波形蛋白表达呈正相关。敲除KLF4表达可促进EMT，并在体外和体内促进胰腺癌细胞的生长和转移。另外，免疫组化（IHC）结果表明KLF4表达与Cav-1表达负相关。此外，下调KLF4表达可增加Cav-1和波形蛋白的表达，并降低E-钙粘蛋白的表达。从机制上讲，KLF4可以通过直接结合Cav-1的启动子域来转录抑制Cav-1的表达。结论KLF4通过下调Cav-1的表达抑制胰腺癌的EMT和转移，提示KLF4 / Cav-1的信号通路可能是新的诊断和治疗靶点。

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