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CECR2 Drives Breast Cancer Metastasis by Suppressing Macrophage Inflammatory Responses

ABSTRACT: CECR2 Drives Breast Cancer Metastasis by Suppressing Macrophage Inflammatory Responses

PROVIDER: PRJNA770272 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16290063_1.fastq.gz	Fastqsanger.gz
	SRR16290063_2.fastq.gz	Fastqsanger.gz
	SRR16290064_1.fastq.gz	Fastqsanger.gz
	SRR16290064_2.fastq.gz	Fastqsanger.gz
	SRR16290065_1.fastq.gz	Fastqsanger.gz

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CECR2 Drives Breast Cancer Metastasis by Suppressing Macrophage Inflammatory Responses

Project description:Purpose: Metastasis are responsible for the most majority of cancer-related deaths due to the lack of effective targeted therapies. Therefore, specific targets which tackle that complex process are needed to improve the therapeutic outcomes of metastatic breast cancer. Methods: ATAC-Seq analysis of CECR2 knockout and control LM2 cells. Results: CECR2 knockout regulate chromatin accessibility of NF-kB target genes . Conclusions: Our work confirmed that CECR2 knockout attenuates chromatin accessibility at promoters or enhancers of the downstream NF-kB target genes.

2022-01-21 | GSE185647 | GEO

Acetyl-lysine Reader CECR2 Drives Breast Cancer Metastasis by Coordinating Macrophage Polarization and Immune Suppression [metastasis]

Project description:Purpose: Advanced breast cancer leads to significantly higher mortality due to metastasis. The goal of this work is to screen and study the deregulated epigenetic regulators to identify the novel targets for the treatment of metastatic breast cancer. Methods:RNA-Seq analysis of matched primary and metastatic breast samples to detect the deregulated epigenetic regulators. Live imaging system was applied to modulate metastatic tumor growth in vivo. Results: we identified that deregulated CECR2 was associated with breast cancer metastasis by RNA sequencing analysis of the matched primary and metastatic breast cancer samples from 13 patients. CECR2 knockout significantly decreased breast cancer metastasis in both immunocompromised and immunocompetent mice models. RNA-seq analysis showed that gene set "response to NF-κB signaling" was significantly decreased by CECR2 depletion in breast cancer cells. Mechanistically, CECR2 formed a complex with RELA on NF-κB target gene promoters to activate target gene expression. Furthermore, CECR2 played a key role in tumor associated macrophage recruitment and polarization, which regulates the antitumor immunity in microenvironment. Conclusions: our work identified and characterized a novel epigenetic regulator CECR2 in regulating breast cancer metastasis, and can serve as a potential target for the treatment of metastatic breast cancer.

2021-12-31 | GSE147995 | GEO

Acetyl-lysine Reader CECR2 Drives Breast Cancer Metastasis by Coordinating Macrophage Polarization and Immune Suppression [cell line]

2021-12-31 | GSE147993 | GEO

Acetyl-lysine Reader CECR2 Drives Breast Cancer Metastasis by Coordinating Macrophage Polarization and Immune Suppression [metastasis]

Project description:Acetyl-lysine Reader CECR2 Drives Breast Cancer Metastasis by Coordinating Macrophage Polarization and Immune Suppression [metastasis]

| PRJNA622783 | ENA

Acetyl-lysine Reader CECR2 Drives Breast Cancer Metastasis by Coordinating Macrophage Polarization and Immune Suppression

Project description:Acetyl-lysine Reader CECR2 Drives Breast Cancer Metastasis by Coordinating Macrophage Polarization and Immune Suppression

| PRJNA622795 | ENA

Acetyl-lysine Reader CECR2 Drives Breast Cancer Metastasis by Coordinating Macrophage Polarization and Immune Suppression [cell line]

Project description:Acetyl-lysine Reader CECR2 Drives Breast Cancer Metastasis by Coordinating Macrophage Polarization and Immune Suppression [cell line]

| PRJNA622775 | ENA

CECR2 drives breast cancer metastasis by promoting NF-κB signaling and macrophage-mediated immune suppression.

Project description:Metastasis is the major cause of cancer-related deaths due to the lack of effective therapies. Emerging evidence suggests that certain epigenetic and transcriptional regulators drive cancer metastasis and could be targeted for metastasis treatment. To identify epigenetic regulators of breast cancer metastasis, we profiled the transcriptomes of matched pairs of primary breast tumors and metastases from human patients. We found that distant metastases are more immune inert with increased M2 macrophages compared to their matched primary tumors. The acetyl-lysine reader, cat eye syndrome chromosome region candidate 2 (CECR2), was the top up-regulated epigenetic regulator in metastases associated with an increased abundance of M2 macrophages and worse metastasis-free survival. CECR2 was required for breast cancer metastasis in multiple mouse models, with more profound effect in the immunocompetent setting. Mechanistically, the nuclear factor κB (NF-κB) family member v-rel avian reticuloendotheliosis viral oncogene homolog A (RELA) recruits CECR2 to increase chromatin accessibility and activate the expression of their target genes. These target genes include multiple metastasis-promoting genes, such as TNC, MMP2, and VEGFA, and cytokine genes CSF1 and CXCL1, which are critical for immunosuppression at metastatic sites. Consistent with these results, pharmacological inhibition of CECR2 bromodomain impeded NF-κB-mediated immune suppression by macrophages and inhibited breast cancer metastasis. These results reveal that targeting CECR2 may be a strategy to treat metastatic breast cancer.

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Cecr2 promotes somatic cell reprogramming as a downstream target of SALL4 [ATAC-seq]

Project description:Sall4 is among one of the most important reprogramming factors. However, the underline molecular mechanisms for such importance remains unclear. In this report, we first described the gene expression and chromatin accessibility dynamics in OKS-Sall4 induced somatic cell reprogramming, and screened a group of downstream targets of Sall4, among which, cecr2, regulated by Sall4 directly, can significantly promote OKS induced reprogramming. Moreover, Cecr2 and Sall4 shared several downstream targets, such as Esrrb, Nanog, T etc., at transcription level when overexpress in the context of OKS induced reprogramming. We further showed that the DTT domain of cecr2 was responding to the reprogramming activity. Our findings provide a new important reprogramming factors and suggesting the cecr2-associted protein network may contributes to overcoming the epigenetic barriers in reprogramming.

2021-03-23 | GSE147678 | GEO

Cecr2 promotes somatic cell reprogramming as a downstream target of SALL4 [ChIP-seq]

2021-03-23 | GSE147680 | GEO

Cecr2 promotes somatic cell reprogramming as a downstream target of SALL4 [RNA-seq]

2021-03-23 | GSE147679 | GEO