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A tumor suppressive-molecular axis EP300/circRERE/miR-6837-3p/MAVS activates type I interferon pathway and anti-tumor immunity to suppress colorectal cancer

ABSTRACT: A tumor suppressive-molecular axis EP300/circRERE/miR-6837-3p/MAVS activates type I interferon pathway and anti-tumor immunity to suppress colorectal cancer

PROVIDER: PRJNA932319 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23362142_1.fastq.gz	Fastqsanger.gz
	SRR23362142_2.fastq.gz	Fastqsanger.gz
	SRR23362143_1.fastq.gz	Fastqsanger.gz
	SRR23362143_2.fastq.gz	Fastqsanger.gz
	SRR23362144_1.fastq.gz	Fastqsanger.gz

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A tumor suppressive-molecular axis EP300/circRERE/miR-6837-3p/MAVS activates type I interferon pathway and anti-tumor immunity to suppress colorectal cancer

Project description:Purpose: The oncogenic role of circRNAs has been well-studied in cancers including colorectal cancer (CRC). However, tumor-suppressive circRNAs and the mechanism through which they exert their anti-tumor effects remain largely unknown. We aim to find out the critical tumor-suppressive circRNAs and their possibility to serve as gene therapy targets. Experimental Design: CircRNA sequencing, gain- and loss- of function experiments，and transcriptomic analysis were performed to find tumor-suppressive and anti-tumor immunity effects of circRERE. Molecular biology experiments were conducted for mechanism exploration. Finally, we conducted adeno-associated virus to deliver circRERE (circRERE-AAV) and evaluated circRERE-AAV alone and in combination with anti-PD-1 antibody in C57BL/6J mice bearing subcutaneous MC38 tumors. Results: CircRERE is lowly expressed in CRC and its lower expression predicts worse prognosis of CRC patients in clinic. Overexpression of circRERE inhibits the malignant behaviors of CRC in vitro and in vivo, while knockdown exhibits the opposite effects. The expression of circRERE is regulated by EP300, a histone acetyltransferase downregulated in CRC as well. Mechanistically, circRERE acts as a ceRNA to sponge miR-6837-3p to upregulate MAVS expression, thereby activating type I IFN signaling and promoting anti-tumor immunity. Delivery of circRERE-AAV elicits significant anti-tumor effects, and combination treatment with circRERE-AAV and anti-PD-1 antibody exhibits synergistic effects on tumor growth in preclinical models of CRC. Conclusions: These results uncover modulatory axis constituting of EP300/circRERE/miR-6837-3p/MAVS and its essential roles in anti-tumor immunity, and demonstrate that circRERE-AAV might represent a new therapeutic avenue to prime immune responses and boost the effects of immunotherapy in clinic.

2023-03-17 | GSE224734 | GEO

A Tumor-suppressive Molecular Axis EP300/circRERE/miR-6837-3p/MAVS Activates Type I IFN Pathway and Antitumor Immunity to Suppress Colorectal Cancer.

Project description:PurposeThe oncogenic role of circular RNAs (circRNA) has been well studied in cancers including colorectal cancer. However, tumor-suppressive circRNAs and the mechanism through which they exert their antitumor effects remain largely unknown. We aim to find out the critical tumor-suppressive circRNAs and their possibility to serve as gene therapy targets.Experimental designcircRNA sequencing, gain-of-function and loss-of-function experiments, and transcriptomic analysis were performed to find tumor-suppressive and antitumor immunity effects of circRERE. Molecular biology experiments were conducted for mechanism exploration. Finally, we conducted adeno-associated virus (AAV) to deliver circRERE (circRERE-AAV) and evaluated circRERE-AAV alone and in combination with anti-PD-1 antibody in C57BL/6J mice bearing subcutaneous MC38 tumors.ResultscircRERE is lowly expressed in colorectal cancer. Overexpression of circRERE inhibits the malignant behaviors of colorectal cancer in vitro and in vivo, while knockdown exhibits the opposite effects. The expression of circRERE is regulated by EP300, a histone acetyltransferase downregulated in colorectal cancer as well. Mechanistically, circRERE acts as a competitive endogenous RNA to sponge miR-6837-3p to upregulate MAVS expression, thereby activating type I IFN signaling and promoting antitumor immunity. Delivery of circRERE-AAV elicits significant antitumor effects, and combination treatment with circRERE-AAV and anti-PD-1 antibody exhibits synergistic effects on tumor growth in preclinical models of colorectal cancer.ConclusionsThese results uncover modulatory axis constituting of EP300/circRERE/miR-6837-3p/MAVS and its essential roles in antitumor immunity, and demonstrate that circRERE-AAV might represent a new therapeutic avenue to prime immune responses and boost the effects of immunotherapy in clinic.

| S-EPMC10233356 | biostudies-literature

Noncanonical MAVS signaling restrains dendritic cell-driven antitumor immunity by inhibiting IL-12

Project description:MAVS-mediated cytosolic RNA sensing plays a central role in tumor immunogenicity. However, the effects of host MAVS signaling on antitumor immunity remains uncertain. Here, we demonstrate that host MAVS pathway drives accelerated tumor growth and impairs antitumor immunity, while MAVS knockout in dendritic cells (DCs) promotes tumor-reactive CD8+ T cell responses. Specifically, the CD8+ T cell priming capacity is enhanced by lack of functional MAVS in a type I interferon-independent, but IL-12-dependent, manner. Mechanistically, loss of RIG-I/MAVS cascade activates non-canonical NF-κB pathway and in turn induces IL-12 production by DCs, resulting in CD8+ T cell: DC crosstalk licensed by IFN-γ and IL-12. Moreover, ablation of host MAVS sensitizes tumors to immunotherapy and attenuates radiation resistance, thereby facilitating the maintenance of effector CD8+ T cells. These findings identify that host MAVS pathway acts as an immune checkpoint of DC-driven antitumor immunity, indicating the development of DC-based immunotherapies through MAVS signaling antagonism.

2023-08-15 | GSE236763 | GEO

UTX condensation underlies its tumor suppressive activity

Project description:UTX condensation underlies its tumor suppressive activity

| PRJNA628656 | ENA

Induction of DISE by tumor suppressive microRNAs

Project description:Induction of DISE by tumor suppressive microRNAs

| PRJNA436738 | ENA

Transcriptome analysis of ΔLMP1-MAVS transfected MARC-145 cells

Project description:We found that fuse ΔLMP1 to MAVS could strengthen MAVS mediated inhibition of PRRSV replication in MARC-145 cells. To better understand the biological function of the fusion protein ΔLMP1-MAVS, overall gene expression of MARC-145 cells transfected with ΔLMP1-MAVS or MAVS was evaluated by mRNA-seq. The result showed that ΔLMP1-MAVS upregulated a number of genes associated with innate immune responses to viral infection, including plenty of interferon-stimulated genes. This study provides reference date to research the working mechanism of ΔLMP1-MAVS.

2019-03-05 | GSE111530 | GEO

Tumor suppressive role of CELF2 in skin tumorignesis

Project description:Tumor suppressive role of CELF2 in skin tumorignesis

| PRJNA1025023 | ENA

Cellular RNA interacts with MAVS to promote antiviral signaling

Project description:Immune signaling needs to be well-regulated to promote clearance of pathogens, while preventing aberrant inflammation. Interferons (IFNs) and antiviral genes are activated by the detection of viral RNA by RIG-I-like receptors (RLRs). Signal transduction downstream of RLRs proceeds through a multiprotein complex organized around the central adaptor protein MAVS. While protein-protein interactions and post-translational modifications are critical for the formation of the MAVS signalosome, whether RNA play a role in organizing these platforms is largely unknown. RNA can modulate protein complex function by allosteric regulation or by serving as a molecular guide or scaffold. We have found that MAVS directly interacts with the 3’ untranslated regions of cellular mRNAs through its central intrinsically disordered domain. Eliminating RNA by RNase treatment disrupts the MAVS signalosome and inhibits phosphorylation of the transcription factor IRF3. These findings support the hypothesis that RNA molecules scaffold the MAVS signaling platform to induce IFNs. Indeed, RNase treatment alters interactions between MAVS and newly identified regulators of RLR signaling. Together, this work uncovers a function for cellular RNA in promoting signaling through MAVS and highlights a generalizable principle of RNA regulatory control of cytoplasmic immune signaling complexes.

2025-03-19 | GSE244000 | GEO

TAZ facilitates breast tumor growth by promoting an immune-suppressive tumor microenvironment

Project description:TAZ facilitates breast tumor growth by promoting an immune-suppressive tumor microenvironment

| PRJNA1011907 | ENA

Modification of Human MAVS protein

Project description:This modification plays a critical role in regulating protein function and cellular processes.MAVS succination sites were identified using mass spectrometry (MS). Identify succination sites of human MAVS protein.

2025-05-26 | PXD061060 | Pride

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