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ETS1 induction by the omental microenvironment promotes ovarian cancer metastasis [RNA-Seq]

ABSTRACT: ETS1 expression is induced by the microenvironment of ovarian metastasis and this expression allows ETS1 to activate a gene expression program involved in cell invasion and epithelial mesenchymal transision.

ORGANISM(S): Homo sapiens

PROVIDER: GSE101833 | GEO | 2018/07/24

REPOSITORIES: GEO

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ETS1 induction by the omental microenvironment promotes ovarian cancer metastasis [ChIP-Seq]

Project description:ETS1 expression is induced by the microenvironment of ovarian metastasis and this expression allows ETS1 to activate a gene expression program involved in cell invasion and epithelial mesenchymal transision.

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ETS1 induction by the omental microenvironment promotes ovarian cancer metastasis

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Laminins in tumor-derived exosomes upregulated by ETS1 reprogram omental macrophages to promote omental metastasis of ovarian cancer.

Project description:Tumor-derived exosomes participate in omental metastatic colonization of ovarian cancer by inducing an adaptive response in the tumor microenvironment. However, cell-cell communication via exosomes between primary tumor cells and the microenvironment of distant omentum and the mechanism of pre-metastatic niche formation are poorly understood. Here, we demonstrated that ETS1-overexpressing ovarian cancer cells secreted larger exosomes with higher laminin levels. In addition, ovarian cancer exosomes could be taken up by omental macrophages through integrin and laminin interaction. Compared with control exosomes, exosomes derived from ETS1-overexpressing ovarian cancer cells (LV-ETS1 Exos) stimulated the polarization of more macrophages toward the M2 phenotype (CD163 marker), as well as the production of more CXCL5 and CCL2 in macrophages, via integrin αvβ5/AKT/Sp1 signaling. In vivo experiments showed that LV-ETS1 Exos promoted omental metastasis of ovarian cancer by mediating the tumor-promoting effect of macrophages, which could be neutralized by integrin ανβ5 inhibitor cilengitide. These results indicated that ETS1 could drive ovarian cancer cells to release exosomes with higher laminin levels, thereby accelerating the exosome-mediated pro-metastatic effects of omental macrophages via the integrin αvβ5/AKT/Sp1 signaling pathway, and the integrin ανβ5 inhibitor cilengitide could inhibit omental metastasis of ovarian cancer driven by tumor-derived exosomes.

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Omental preadipocytes stimulate matrix remodeling and IGF signaling to support ovarian cancer metastasis

Project description:Ovarian cancer can metastasize to the omentum, which is associated with a complex tumor microenvironment. Omental stromal cells facilitate ovarian cancer colonization by secreting cytokines and growth factors. Improved understanding of the tumor supportive functions of specific cell populations in the omentum could identify strategies to prevent and treat ovarian cancer metastasis. Here, we showed that omental preadipocytes enhance the tumor initiation capacity of ovarian cancer cells. Secreted factors from preadipocytes supported cancer cell viability during nutrient and isolation stress and enabled prolonged proliferation. Co-culturing with pre-adipocytes led to upregulation of genes involved in extracellular matrix (ECM) organization, cellular response to stress, and regulation of insulin-like growth factor (IGF) signaling in ovarian cancer cells. IGF-1 induced ECM genes and increased alternative NF-κB signaling by activating RelB. Inhibiting the IGF-1 receptor (IGF1R) initially increased tumor omental adhesion but decreased growth of established preadipocyte-induced subcutaneous tumors as well as established intraperitoneal tumors. Together, this study shows that omental preadipocytes support ovarian cancer progression, which has implications for targeting metastasis.

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Ets-1 over-expression in ovarian cancer cells

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Expression data of Rag2-deficient Ets1++ and Rag2-deficient Ets1-- mature NK cells and WT bone marrow progenitors

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Effect of Ets1 knockdown in the P5424 thymic cell line

Project description:We performed ChIP-Seq for Ets1 and histone modifications in P5424 thymic cells, without and with Ets1 knockdown via shRNA. Overall, we find that loss of Ets1 results in specific, higher occupancy of H3K4me1-marked nucleosomes at the Ets1 binding site, but not H3K4me3 nucleosomes. We verified the specificity of this mechanism as Ets1-dependent by also computing H3K4me1 and 3 nucleosome occupancy in hypersensitive, Ets1-depleted sites. This effect was also found in primary WT DN+DP Ets1 sites. Overall, this suggests that Ets1 induces chromatin remodeling and that its loss increases H3K4me1 nucleosome occupancy in bound sites, with levels of H3K4me3 comparatively unchanged, thus reducing the activation status of these enhancers Genome-wide analysis via ChIP-Seq for Ets1, H3K4me1 and H3K4me3 in WT, sh-scramble and sh-Ets1 the P5424 thymic cell line

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ETS1 and ETS2

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