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Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in small cell lung cancer (RNA-Seq)

ABSTRACT: Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in small cell lung cancer (RNA-Seq)

PROVIDER: PRJNA1080567 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28097741.fastq.gz	Fastqsanger.gz
	SRR28097742.fastq.gz	Fastqsanger.gz
	SRR28097743.fastq.gz	Fastqsanger.gz

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Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in small cell lung cancer (ChIP-Seq)

Project description:Small-cell lung cancer (SCLC) is the most aggressive and lethal type of lung cancer, characterized by limited treatment options, early and frequent metastasis. However, the determinants of metastasis in SCLC are poorly defined. Here, we show that estrogen-related receptor gamma (ERRγ) is overexpressed in metastatic SCLC tumors, and it is positively associated with SCLC progression. ERRγ functions as an essential activator of ECM remodeling and cell adhesion, two critical steps in metastasis, by directly regulating the expression of major genes involved in these processes. Genetic and pharmacological inhibition of ERRγ markedly reduces collagen production, cell-matrix adhesion, microfilaments production, and eventually blocks SCLC cell invasion and tumor metastasis. Notably, ERRγ antagonists significantly suppress tumor growth and metastasis and restore resistant SCLC vulnerability to chemotherapy in multiple cell-derived and patient-derived xenograft models. Taken together, these findings establish ERRγ as an attractive target for metastatic SCLC and provide a potential pharmacological strategy for treating this lethal disease.

2024-05-15 | GSE259272 | GEO

Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in small cell lung cancer (RNA-Seq)

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Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in small cell lung cancer

Project description:Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in small cell lung cancer

| PRJNA1080561 | ENA

Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in small cell lung cancer (ChIP-Seq)

Project description:Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in small cell lung cancer (ChIP-Seq)

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Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in small cell lung cancer.

Project description: Not available

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Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in SCLC

Project description: Not available

| S-SCDT-10_1038-S44321-024-00108-Z | biostudies-other

Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in small cell lung cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-17 | GSE259273 | GEO

A combinatorial extracellular matrix platform identifies cell-extracellular matrix interactions that correlate with metastasis

Project description:Extracellular matrix interactions play essential roles in normal physiology and many pathological processes. Here, we report a novel screening platform capable of measuring phenotypic responses to combinations of ECM molecules. While the importance of ECM interactions in metastasis is well documented, systematic approaches to identify their roles in distinct stages of tumorigenesis have not been described. Using a genetic mouse model of lung adenocarcinoma, we measured the ECM-dependent adhesion of tumor-derived cells. Hierarchical clustering of adhesion profiles generated using this platform differentially segregated metastatic cell lines from primary tumor lines. Furthermore, we uncovered that metastatic cells selectively associate with fibronectin when in combination with galectin-3, galectin-8, or laminin. These interactions appear to be mediated in part by Î±3Î²1 integrin both in vitro and in vivo. We show that these galectins also correlate with human disease at both a transcriptional and histological level. Thus, our in vitro platform allowed us to interrogate the interactions of metastatic cells with their surrounding environment, and identified ECM and integrin interactions that could lead to therapeutic targets for metastasis prevention. Cell lines derived from murine lung primary adenocarcinomas and their metastases (Winslow et al., 2011 Nature 473:101-104)

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Specific extracellular matrix remodeling signature of colon hepatic metastases

Project description:To identify genes implicated in metastatic colonization of the liver in colorectal cancer, we collected pairs of primary tumors and hepatic metastases before chemotherapy in 13 patients. We compared mRNA expression in the pairs of patients to identify genes deregulated during metastatic evolution. We then validated the identified genes using data obtained by different groups. The 33-gene signature was able to classify 87% of hepatic metastases, 98% of primary tumors, 97% of normal colon mucosa, and 95% of normal liver tissues in six datasets obtained using five different microarray platforms. The identified genes are specific to colon cancer and hepatic metastases since other metastatic locations and hepatic metastases originating from breast cancer were not classified by the signature. Gene Ontology term analysis showed that 50% of the genes are implicated in extracellular matrix remodeling, and more precisely in cell adhesion, extracellular matrix organization and angiogenesis. Because of the high efficiency of the signature to classify colon hepatic metastases, the identified genes represent promising targets to develop new therapies that will specifically affect hepatic metastasis microenvironment. 57 samples of patients with stage IV colorectal cancer. We compared using Affymetrix chips gene expression profiles between primary tumors and hepatic metastases

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Histone Demethylase KDM4A Activates ERRγ-Dependent Cell Cycle Progression to Promote Endometrial Cancer Progression

Project description:Endometrial cancer is driven by complex genetic and epigenetic alterations, yet the key chromatin-dependent mechanisms sustaining malignant proliferation remain incompletely defined. Here, we report that lysine demethylase 4A (KDM4A) is aberrantly upregulated in endometrial cancer cells and promotes aggressive growth by epigenetically activating estrogen-related receptor γ (ERRγ). Mechanistically, KDM4A binds to the ERRγ promoter and, through its histone demethylase activity, selectively removes the repressive H3K9me3 mark, thereby relieving transcriptional silencing and elevating ERRγ expression. Functionally, ERRγ acts as a downstream transcription factor that enhances the transcription and protein abundance of cell cycle–associated regulators, facilitating the G2-to-M phase transition and accelerating malignant proliferation. Importantly, pharmacological inhibition of KDM4A using JIB-04 markedly suppresses tumor growth both in vitro and in vivo, concomitant with restoration of H3K9me3 enrichment at the ERRγ promoter, downregulation of ERRγ and its cell cycle gene program, and induction of G2/M arrest. Together, our findings establish a KDM4A–H3K9me3–ERRγ signaling cascade that links epigenetic derepression to cell cycle progression in endometrial cancer, and they provide preclinical evidence that targeting KDM4A with JIB-04 represents a promising therapeutic strategy to curb endometrial cancer proliferation.

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