FOXF1 Induces Epithelial-Mesenchymal Transition in Colorectal Cancer Metastasis by Transcriptionally Activating SNAI1.

Abstract:

: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.

journal_name

Neoplasia

authors

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

doi

10.1016/j.neo.2018.08.004

subject

Has Abstract

pub_date

2018-10-01 00:00:00

pages

996-1007

issue

10

eissn

1522-8002

issn

1476-5586

pii

S1476-5586(18)30367-1

journal_volume

20

pub_type

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