FOXF1 Induces Epithelial-Mesenchymal Transition in Colorectal Cancer Metastasis by Transcriptionally Activating SNAI1.
FOXF1 Induces Epithelial-Mesenchymal Transition in Colorectal Cancer Metastasis by Transcriptionally Activating SNAI1.
复制标题
FOXF1 通过转录激活 SNAI1 诱导结直肠癌转移中的上皮间质转化
DOI：
10.1016/j.neo.2018.08.004
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发表时间：
2018-10
期刊：
影响因子：
--
通讯作者：
Ye Y
中科院分区：
文献类型：
--
作者：
Wang S;Yan S;Zhu S;Zhao Y;Yan J;Xiao Z;Bi J;Qiu J;Zhang D;Hong Z;Zhang L;Huang C;Li T;Liang L;Liao W;Jiao H;Ding Y;Ye Y
叉头盒F1（FOXF1）最近被认为与肺癌和乳腺癌的癌症进展和转移有关。然而，FOXF1在调节结直肠癌（CRC）进展中的生物学功能和潜在机制在很大程度上是未知的。我们发现FOXF1在93例石蜡包埋的结直肠癌组织中表达上调，FOXF1的高表达和核定位与结直肠癌患者的侵袭性特征和较差的生存率显著相关。GSEA分析表明，FOXF1的高水平与EMT基因标签的富集呈正相关，FOXF1的外源性过表达通过转录激活SNAI1诱导EMT。外源性过表达FOXF1在功能上促进CRC细胞的侵袭和转移特征，并且抑制SNAI1减弱FOXF1过表达CRC细胞的侵袭表型和转移潜力。组织芯片检测结果显示FOXF1和SNAI1在大肠癌组织中的表达呈正相关。这些结果表明FOXF1通过转录激活SNAI1诱导EMT在CRC转移中起关键作用，突出了CRC的潜在新治疗策略。
Forkhead Box F1 (FOXF1) has been recently implicated in cancer progression and metastasis of lung cancer and breast cancer. However, the biological functions and underlying mechanisms of FOXF1 in the regulation of the progression of colorectal cancer (CRC) are largely unknown. We showed that FOXF1 was up-regulated in 93 paraffin-embedded archived human CRC tissue, and both high expression and nuclear location of FOXF1 were significantly associated with the aggressive characteristics and poorer survival of CRC patients. The GSEA analysis showed that the higher level of FOXF1 was positively associated with an enrichment of EMT gene signatures, and exogenous overexpression of FOXF1 induced EMT by transcriptionally activating SNAI1. Exogenous overexpression FOXF1 functionally promoted invasion and metastasis features of CRC cells, and inhibition of SNAI1 attenuates the invasive phenotype and metastatic potential of FOXF1-overexpressing CRC cells. Furthermore, the results of the tissue chip showed that the expression of FOXF1 was positively correlated with SNAI1 in CRC tissues chip. These results suggested that FOXF1 plays a critical role in CRC metastasis by inducing EMT via transcriptional activation of SNAI1, highlighting a potential new therapeutic strategy for CRC.
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