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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE148005 | GEO | 2021/12/31

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

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.

| S-EPMC9003667 | biostudies-literature

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

The Polycomb Repressor Complex 1 Drives Double-Negative Prostate Cancer Metastasis by Coordinating Stemness and Immune Suppression.

Project description:The mechanisms that enable immune evasion at metastatic sites are poorly understood. We show that the Polycomb Repressor Complex 1 (PRC1) drives colonization of the bones and visceral organs in double-negative prostate cancer (DNPC). In vivo genetic screening identifies CCL2 as the top prometastatic gene induced by PRC1. CCL2 governs self-renewal and induces the recruitment of M2-like tumor-associated macrophages and regulatory T cells, thus coordinating metastasis initiation with immune suppression and neoangiogenesis. A catalytic inhibitor of PRC1 cooperates with immune checkpoint therapy to reverse these processes and suppress metastasis in genetically engineered mouse transplantation models of DNPC. These results reveal that PRC1 coordinates stemness with immune evasion and neoangiogenesis and point to the potential clinical utility of targeting PRC1 in DNPC.

| S-EPMC7210785 | biostudies-literature

KIT oncogene inhibition drives intratumoral macrophage M2 polarization.

Project description:Tumor-associated macrophages (TAMs) are a major component of the cancer microenvironment. Modulation of TAMs is under intense investigation because they are thought to be nearly always of the M2 subtype, which supports tumor growth. Gastrointestinal stromal tumor (GIST) is the most common human sarcoma and typically results from an activating mutation in the KIT oncogene. Using a spontaneous mouse model of GIST and 57 freshly procured human GISTs, we discovered that TAMs displayed an M1-like phenotype and function at baseline. In both mice and humans, the KIT oncoprotein inhibitor imatinib polarized TAMs to become M2-like, a process which involved TAM interaction with apoptotic tumor cells leading to the induction of CCAAT/enhancer binding protein (C/EBP) transcription factors. In human GISTs that eventually developed resistance to imatinib, TAMs reverted to an M1-like phenotype and had a similar gene expression profile as TAMs from untreated human GISTs. Therefore, TAM polarization depends on tumor cell oncogene activity and has important implications for immunotherapeutic strategies in human cancers.

| S-EPMC3865475 | biostudies-literature

CECR2 Drives Breast Cancer Metastasis by Suppressing Macrophage Inflammatory Responses

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

| PRJNA770272 | ENA