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ETS1 induction by the omental microenvironment promotes ovarian cancer metastasis

ABSTRACT: ETS1 induction by the omental microenvironment promotes ovarian cancer metastasis

PROVIDER: PRJNA395678 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5865180.fastq.gz	Fastqsanger.gz
	SRR5865190.fastq.gz	Fastqsanger.gz
	SRR5865181.fastq.gz	Fastqsanger.gz
	SRR5865182.fastq.gz	Fastqsanger.gz
	SRR5865183.fastq.gz	Fastqsanger.gz

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

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ETS1 induction by the omental microenvironment promotes ovarian cancer metastasis

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

Project description: Not available

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Matched primary ovarian cancer, omental metastases, and non-omental metastases from 10 patients with high-grade serous ovarian carcinoma

Project description:Matched high-grade serous ovarian carcinoma samples collected from the ovary (ov), omental metastasis (om-met), and non-omental intraperitoneal metastasis (met) from 10 patients at the time of primary debulking surgery were analyzed for RNA expression by RNA sequencing.

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Homo sapiens

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

| PRJNA395682 | ENA

Homo sapiens

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

| PRJNA395683 | ENA

ETS1 Orchestrates a Hybrid EMT Program Driving in vivo Metastasis and Immune Evasion

Project description:Transcriptional Intratumoral heterogeneity (ITH) is a hallmark of aggressive cancers, yet how transcriptional ITH programs drive tumor metastasis and immune evasion in upper aerodigestive squamous cell carcinoma (UASCC) remains unclear. Through single-cell RNA sequencing analysis of UASCC cells and patient tumors, we uncovered a hybrid EMT (hEMT) ITH program linked to metastatic dissemination. The transcription factor ETS1 was identified as a master regulator of hEMT program, directly activating pro-metastatic genes and promoting distant spread in vivo. Unexpectedly, ETS1 also orchestrated an immune-cold tumor microenvironment by transcriptionally activating the STAT1-PDL1 axis, suppressing T lymphocyte infiltration and elevating immune checkpoint molecules. Clinically, ETS1-high tumors strongly correlated with poor survival and resistance to immune checkpoint blockade across multiple cohorts. Leveraging drug screens, we discovered that ETS1-high cancers are vulnerable to HSP90 inhibitors (e.g., Alvespimycin), which suppress ETS1 by disrupting HIF1A-mediated transcriptional activation. Together, our work reveals ETS1 as a dual driver of tumor distal metastasis and immune evasion in UASCC, while nominating HSP90 inhibition as a tailored strategy for ETS1-driven tumors. These findings provide a roadmap for targeting aggressive ITH subsets and overcoming immunotherapy resistance.

2026-05-08 | GSE300573 | GEO

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Project description:Omentum is one of the most preferred metastatic sites in patients with high-grade serous ovarian cancer, while the underlying mechanisms remain poorly understood. Here, we aim to identify biomarkers related to omental metastasis in high-grade serous ovarian cancer. In this study, we constructed a risk model comprising FAM9A, BARX1, SNORA79, CIDEA, FABP4, and TRARG1 as risk factors for omental metastasis using the machine-learning methods LASSO and Random Forest. And we identified BARX1 (BarH-like homeobox 1) as the gene with the highest predictive value. Further studies validated the high expression of BARX1 across pan-cancers and its association with immune cell infiltration using CIBERSORT analysis. Our research underscores the crucial role of BARX1 in OC and highlights its potential as a therapeutic target.

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