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CECR2 Drives Breast Cancer Metastasis by Suppressing Macrophage Inflammatory Responses

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE185647 | GEO | 2022/01/21

REPOSITORIES: GEO

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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

Cecr2 promotes somatic cell reprogramming as a downstream target of SALL4 [RNA-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 | GSE147679 | GEO

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

2021-03-23 | GSE147678 | GEO

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

2021-03-23 | GSE147680 | GEO

CECR2 Drives Breast Cancer Metastasis by Suppressing Macrophage Inflammatory Responses

Project description:CECR2 Drives Breast Cancer Metastasis by Suppressing Macrophage Inflammatory Responses

| PRJNA770272 | ENA

A novel YDDX linear motif mediates docking of the IKK kinase to substrates: structural and functional insights

Project description:The inhibitor of kB kinase (IKK) is the master regulator of the nuclear factor kB (NF-kB) pathway, involved in inflammatory, immune and apoptotic responses. In the ‘canonical’ NF-kB pathway, IKK phosphorylates inhibitor of kB (IkB) proteins and this triggers ubiquitin-mediated degradation of IkB, leading to release and nuclear translocation of NF-B transcription factors. The data presented show that the IKK and IKK subunits recognize a YDDX docking site located within the disordered C-terminal region of IkBa. Our results also suggest that IKK contributes to the docking interaction with higher affinity as compared to IKK.

2024-05-09 | PXD037534 | JPOST Repository

RNA sequencing of NF-kB knockout (KO) U937 cells

Project description:RNA sequencing of NF-kB knockout (KO) U937 cells

| PRJNA641643 | ENA

Coactivation of NF-kB and Notch signaling is sufficient to induce B cell transformation and enables B-myeloid conversion

Project description:Comparison of chromatin accessibility between NF-kB and Notch coactivated marginal zone precursor (MZP) B cells and converted myeloid cells from these B cells

2020-08-01 | GSE136408 | GEO

Dynamic Chromatin Localization of Sirt6 Shapes Stress- and Aging- Related Transcriptional Networks (ChIP-chip)

Project description:Sirtuins (Sirt) are a family of enzymes that modify chromatin and other proteins to affect gene activity. Loss of Sirt6 leads to a progeria-like phenotype in mice, but the target of SIRT6 action has been elusive. Here we show that Sirt6 binds to thousands of gene promoters in a stress-inducible fashion, guided by the stress-responsive transcription factor NF-?B. Chromatin profiling by ChIP-chip analysis of Sirt6 and NF-KB component RelA combined with expression array data of wildtype, Sirt6 knockout and Sirt6 RelA double knockout cells demonstrates that RelA recruits Sirt6 to NF-KB targets in response to TNF-a induction and that many of these targets are important for senescence and aging. comparison of wild type, RelA -/- and Sirt6-/- MEF cells

2011-05-11 | E-GEOD-28638 | biostudies-arrayexpress

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