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Runx/CBFβ transcription factor complexes regulate Ccl5 expression through two novel enhancers to enhance tumor immunity [dataset 3]

ABSTRACT: Runx/CBFβ transcription factor complexes regulate Ccl5 expression through two novel enhancers to enhance tumor immunity [dataset 3]

PROVIDER: PRJNA554314 | ENA |

REPOSITORIES: ENA

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Runx/CBFβ transcription factor complexes regulate Ccl5 expression through two novel enhancers to enhance tumor immunity

Project description:Runx/CBFβ transcription factor complexes regulate Ccl5 expression through two novel enhancers to enhance tumor immunity

| PRJNA540714 | ENA

Runx/CBFβ transcription factor complexes regulate Ccl5 expression through two novel enhancers to enhance tumor immunity [dataset 3]

Project description:CCL5 (also known as RANTES) was originally known to be important to recruit memory T cells to infected sites, but it received much attention as an inhibitor to HIV’s entry into T lymphocytes of AIDS patients. Recently, it has been reported to be necessary to sustain Trm (Tissue-resident memory) T cells at local tissues as well as to play roles in manipulating tumor microenvironment by both host immunity and cancer cells. Nonetheless, little is known how Ccl5 expression is regulated, thus making it quite difficult for therapeutic intervention. Our study reveals that Runx/CBFβ transcription factor complexes antagonizes Ccl5 expression through two novel transcriptional enhancers. The proximal enhancer is required for the homeostatic expression of Ccl5 during the steady state, meanwhile the distal enhancer is necessary for the expression Ccl5 during the activated stage. We employed enChIP-seq to identify the distal enhancer located 1.35 Mb away from the promoter. This long distance interaction requires the help from Satb1, a global chromatin organizer. Our study reveals that the reduced amounts of Ccl5 by the deletion of the proximal enhancer results in an enhancement of metastasis in B16-F10 melanoma model. On the other hand, a Runx3-mutant mouse line in which Ccl5 expression is increased showed the opposite outcome, suggesting a novel inverse correlation between host Ccl5 levels and metastasis rate.

2019-07-12 | GSE134206 | GEO

Runx/CBFβ transcription factor complexes regulate Ccl5 expression through two novel enhancers to enhance tumor immunity [dataset 1]

Project description:CCL5 (also known as RANTES) was originally known to be important to recruit memory T cells to infected sites, but it received much attention as an inhibitor to HIV’s entry into T lymphocytes of AIDS patients. Recently, it has been reported to be necessary to sustain Trm (Tissue-resident memory) T cells at local tissues as well as to play roles in manuplating tumor microenvironment by both host immunity and cancer cells. Nonetheless, little is known how Ccl5 expression is regulated, thus making it quite difficult for therapeutic intervention. Our study reveals that Runx/CBFβ transcription factor complexes antagonizes Ccl5 epxression through two novel transcriptional enhancers. The proximal enhancer is required for the homeostatic expression of Ccl5 during the steady state, meanwhile the distal enhancer is necessary for the expression Ccl5 during the activated stage. We employed enChIP-seq to identify the distal enhancer located 1.35 Mb away from the promoter. This long distance interaction requires the help from Satb1, a global chromatin organizer. Our study reveals that the redeced amounts of Ccl5 by the deletion of the proximal enhancer results in an enhancement of metastasis in B16-F10 melanoma model. On the other hand, a Runx3-mutant mouse line in which Ccl5 expression is increased showed the opposite outcome, suggesting a novel inverse correlation between host Ccl5 levels and metastasis rate.

2019-04-25 | GSE130235 | GEO

Runx/CBFβ transcription factor complexes regulate Ccl5 expression through two novel enhancers to enhance tumor immunity [dataset 2]

2019-05-01 | GSE130599 | GEO

Runx/CBFβ transcription factor complexes regulate Ccl5 expression through two novel enhancers to enhance tumor immunity [dataset 1]

Project description:Runx/CBFβ transcription factor complexes regulate Ccl5 expression through two novel enhancers to enhance tumor immunity [dataset 1]

| PRJNA534422 | ENA

Runx/CBFβ transcription factor complexes regulate Ccl5 expression through two novel enhancers to enhance tumor immunity [dataset 2]

Project description:Runx/CBFβ transcription factor complexes regulate Ccl5 expression through two novel enhancers to enhance tumor immunity [dataset 2]

| PRJNA540715 | ENA

Runx/Cbfβ complexes protect ILC2s from exhaustion during allergic airway inflammation

Project description:Runx/Cbfβ complexes protect ILC2s from exhaustion during allergic airway inflammation

| PRJNA438449 | ENA

Runx/Cbfβ complexes protect ILC2s from exhaustion during allergic airway inflammation

Project description:Group 2 innate lymphoid cells (ILC2s) have tissue-resident competence and contribute to the pathogenesis of allergic diseases. Therefore, there should be mechanisms to maintain the capacity of ILC2s to produce TH2 cytokines under chronic inflammatory conditions. Here, we report that Runx proteins are essential to prevent exaggerated activation of ILC2, in part by antagonizing GATA-3 function at steady state. However, during allergic inflammation, the absence of Runx in ILC2s impaired their ability to proliferate and produce effector TH2 cytokines and chemokines, but instead induced expression of T cell exhaustion markers including IL-10 and TIGIT. These exhausted ILC2s were unabale to induce type 2 immune responses against repeated allergen inhalation. Thus, Runx proteins protect ILC2s from exhaustion during continuous allergic inflammation.

2019-01-07 | GSE111871 | GEO

Runx/CBFβ transcription factor complexes regulate Ccl5 expression through two novel enhancers to enhance tumor immunity

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

2019-05-01 | GSE130600 | GEO

CBFβ promotes colorectal tumor growth and metastasis in a RUNX2-dependent manner (ChIP-seq)

Project description:Transcriptional regulation is critically involved in colorectal cancer (CRC) pathogenesis, the mechanism of which remains incompletely understood. Here, we report that core-binding factor β (CBFβ) is commonly upregulated in human colorectal cancer and is associated with the survival rate of CRC patients. Immunohistochemistry (IHC) analysis of RUNX1-3 expression in CRC patients and other in vitro data revealed that CBFβ promotes cell proliferation and liver metastasis in a RUNX2-dependent way. Transcriptome sequencing, ChIP-seq and promoter-binding experiments demonstrated that the CBFβ/RUNX2 complex could activate the transcription of OPN, FAM129A and UPP1. Furthermore, CBFβ significantly promoted tumor growth and lung metastasis in a mouse xenograft model and an orthotopic liver metastasis model of CRC. Additionally, we identified that tumor-suppressive miR-143/145 could synergistically target CBFβ by specifically binding to its 3’-UTR region. An inverse correlation between miR-143/145 and CBFβ was verified in CRC patients. Our results represent the first report describing a mechanistic role for CBFβ-RUNX2 in the transcriptional activation of OPN, FAM129A and UPP1 in controlling colorectal cancer development, which may offer prognostic and therapeutic opportunities.

2021-11-10 | GSE153682 | GEO

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