Abstract：
:Metastatic colonization involves paracrine/juxtacrine interactions with the microenvironment inducing an adaptive response through transcriptional regulation. However, the identities of transcription factors (TFs) induced by the metastatic microenvironment in ovarian cancer (OC) and their mechanism of action is poorly understood. Using an organotypic 3D culture model recapitulating the early events of metastasis, we identified ETS1 as the most upregulated member of the ETS family of TFs in metastasizing OC cells as they interacted with the microenvironment. ETS1 was regulated by p44/42 MAP kinase signaling activated in the OC cells interacting with mesothelial cells at the metastatic site. Human OC tumors had increased expression of ETS1, which predicted poor prognosis. ETS1 regulated OC metastasis both in vitro and in mouse xenografts. A combination of ChIP-seq and RNA-seq analysis and functional rescue experiments revealed FAK as the key transcriptional target and downstream effector of ETS1. Taken together, our results indicate that ETS1 is an essential transcription factor induced in OC cells by the microenvironment, which promotes metastatic colonization though the transcriptional upregulation of its target FAK.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Tomar S,Plotnik JP,Haley J,Scantland J,Dasari S,Sheikh Z,Emerson R,Lenz D,Hollenhorst PC,Mitra AKdoi
10.1016/j.canlet.2017.11.012subject
Has Abstractpub_date
2018-02-01 00:00:00pages
190-204eissn
0304-3835issn
1872-7980pii
S0304-3835(17)30730-9journal_volume
414pub_type
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