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SHISA3 reprograms tumor-associated macrophages toward an M1 phenotype and enhances cancer immunotherapy

ABSTRACT: SHISA3 reprograms tumor-associated macrophages toward an M1 phenotype and enhances cancer immunotherapy

PROVIDER: PRJNA1076213 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27960535_1.fastq.gz	Fastqsanger.gz
	SRR27960535_2.fastq.gz	Fastqsanger.gz
	SRR27960536_1.fastq.gz	Fastqsanger.gz
	SRR27960536_2.fastq.gz	Fastqsanger.gz
	SRR27960537_1.fastq.gz	Fastqsanger.gz

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SHISA3 reprograms tumor-associated macrophages toward an M1 phenotype and enhances cancer immunotherapy

Project description:The main challenge for immune checkpoint blockade (ICB) therapy lies in immunosuppressive tumor microenvironment (TME). Repolarizing M2-like tumor-associated macrophages (TAMs) into inflammatory M1 phenotype is a promising strategy for cancer immunotherapy. Here, we found that the transmembrane protein SHISA3 is induced by DAMPs/PAMPs in macrophages via nuclear factor-κB (NF-κB) transcription factors, and SHISA3 forms complex with HSPA8 to reciprocally activates NF-κB signaling thus maintains M1 polarization of macrophages. Enforced expression of Shisa3 in TAMs increases their phagocytosis and antigen presentation abilities and promotes CD8+ T cell-mediated antitumor immunity. Local delivery of mRNA encoding Shisa3 enables therapy of cancer by dual effects on tumor cells and TAMs, and enhance the efficacy of PD-1 antibody. Taken together, our findings describe the role of SHISA3 in reprogramming TAMs that ameliorates cancer immunotherapy To find new molecules that regulate macrophage polarization, we performed transcriptomic analysis on early macrophages polarization induced by LPS for 0, 2, 4 hours.

2024-10-02 | GSE255711 | GEO

SHISA3 Reprograms Tumor-Associated Macrophages Toward an Antitumoral Phenotype and Enhances Cancer Immunotherapy.

Project description:The main challenge for immune checkpoint blockade (ICB) therapy lies in immunosuppressive tumor microenvironment (TME). Repolarizing M2-like tumor-associated macrophages (TAMs) into inflammatory M1 phenotype is a promising strategy for cancer immunotherapy. Here, this study shows that the tumor suppressive protein SHISA3 regulates the antitumor functions of TAMs. Local delivery of mRNA encoding Shisa3 enables cancer immunotherapy by reprogramming TAMs toward an antitumoral phenotype, thus enhancing the efficacy of programmed cell death 1 (PD-1) antibody. Enforced expression of Shisa3 in TAMs increases their phagocytosis and antigen presentation abilities and promotes CD8+ T cell-mediated antitumor immunity. The expression of SHISA3 is induced by damage/pathogen-associated molecular patterns (DAMPs/PAMPs) in macrophages via nuclear factor-κB (NF-κB) transcription factors. Reciprocally, SHISA3 forms a complex with heat shock protein family A member 8 (HSPA8) to activate NF-κB signaling thus maintaining M1 polarization of macrophages. Knockout Shisa3 largely abolishes the antitumor efficacy of combination immunotherapy with Toll-like receptor 4 (TLR4) agonist monophosphoryl lipid A (MPLA) and PD-1 antibody. It further found that higher expression of SHISA3 in antitumoral TAMs is associated with better overall survival in lung cancer patients. Taken together, the findings describe the role of SHISA3 in reprogramming TAMs that ameliorate cancer immunotherapy.

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Damage-associated molecular patterns induce macrophage polarization toward an M1 pro-inflammatory phenotype

Project description:Damage-associated molecular patterns induce macrophage polarization toward an M1 pro-inflammatory phenotype

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miR-15a reprograms activated hepatic stellate cells back toward quiescence

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A phosphatase-like nanomaterial promotes autophagy and reprograms macrophage for cancer immunotherapy

Project description:Macrophages are very plastic and play key roles in maintenance of tissue homeostasis. In cancer progression, macrophages also take parts through all the processes, from the initiation, progression, to the final tumor metastasis. Although energy deprivation and autophagy are widely used for cancer therapy, most of these strategies are not meant to target macrophages resulting in undesired effects and unsatisfactory outcomes for cancer immunotherapy. Herein, we developed a lanthanum nickel oxide (LNO) nanozyme that possesses phosphatase-like activity for ATP hydrolysis. Meanwhile, the autophagy of macrophages induced by LNO promotes the polarization of macrophages from M2-like macrophage (M2) to M1-like macrophage (M1) and reduces tumor-associated macrophages in tumor-bearing mice, exhibiting capability of killing tumor-associated macrophage and anti-tumor effect in vivo. Furthermore, pre-coating by myeloid cell membrane on the surface of LNO significantly enhanced antitumor immunity. Our findings demonstrate that phosphatase-like nanozyme, LNO can specifically induce macrophage autophagy that improves therapeutic efficacy and offers valuable strategies for cancer immunotherapy.

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Damage-associated molecular patterns induce macrophage polarization toward an M1 pro-inflammatory phenotype

Project description:Dying cells release Damage-Associated Molecular Patterns (DAMPs) that can initiate and perpetuate sterile inflammatory responses. However, the effect of DAMPs on macrophages biology remains unclear. We therefore studied the effect of DAMPs on primary peritoneal macrophages (PPM) in vitro. We first performed unbiased transcriptomic profiling with RNA-seq of PPMs cultured for up to 72 hours in the presence and absence of: 1) liposaccharide (LPS), which is known to provoke an “M1” phenotype, 2) IL-4, which is known to provoke an “M2” phenotype, or 3) cytosolic extracts (CEs) from necrotic H9C2 cells to mimic the release of cardiomyocyte DAMPs. We found that the transcriptional profile of PPMs stimulated with CEs resembled the transcriptional profile of PPMs stimulated with LPS.

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Project description:Mycobacterium bovis Bacillus Calmette-Guérin (BCG) is the vaccine against tuberculosis and an immunotherapy for bladder cancer. When administered intravenously, BCG reprograms bone marrow hematopoietic stem and progenitor cells (HSPCs), leading to heterologous protection against infections. Whether HSPC reprogramming contributes to the anti-tumor effects of BCG administered into the bladder is unknown. We demonstrate that BCG administered in the bladder colonizes the bone marrow and, in both mice and humans, reprograms HSPCs to alter and amplify myelopoiesis. BCG-reprogrammed HSPCs are sufficient to confer augmented anti-tumor immunity through production of neutrophils, monocytes, and dendritic cells that broadly remodel the tumor microenvironment, drive T cell-dependent anti-tumor responses, and synergize with checkpoint blockade. We conclude that bladder BCG acts systemically through hematopoiesis, highlighting the broad potential of HSPC reprogramming to enhance the innate drivers of T cell-dependent tumor immunity.

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Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Human_Mulitome_Cohort1]

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Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Mouse_Multiome]

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Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Mouse_LSK_ATAC]

2025-04-22 | GSE295004 | GEO