Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hepatocellular carcinoma specific epigenetic checkpoint bi-directionally regulates antitumor immunity of CD4+T cell

ABSTRACT: Hepatocellular carcinoma specific epigenetic checkpoint bi-directionally regulates antitumor immunity of CD4+T cell

PROVIDER: PRJNA1097278 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Oncolytic virus M1 functions as a bi-functional checkpoint inhibitor to enhance the antitumor activity of DC vaccine

Project description:Although promising, dendritic cell (DC) vaccines still provide limited clinical benefits, mainly due to the immunosuppressive tumor microenvironment (TME) and the lack of tumor-associated antigens (TAAs). Oncolytic viruses are considered to be an ideal strategy to overcome immunosuppression and expose TAAs, therefore they may work synergistically with DC vaccines. In this study, we demonstrated that oncolytic virus M1 (OVM) can enhance the antitumor effects of DC vaccine in a variety of syngeneic tumor mouse models by increasing the infiltration of CD8+ effector T cells in the TME. Mechanically, we identified that tumor cells offset the function of DC vaccines through the myeloid immune checkpoint SIRPα-CD47, while OVM can downregulate the expression of SIRPα and CD47 in DCs and tumor cells, respectively. Based on the fact that OVM upregulates the expression of PD-L1 in DCs, PD-L1 blockade was introduced with the combination of DC vaccines and OVM, resulting in a further potentiation of antitumor activity. Overall, we revealed that OVM can strengthen the antitumor efficacy of DC vaccines by targeting the immune checkpoint SIRPα-CD47 axis, which exerts dominant immunosuppressive effects on DC vaccines.

2023-09-01 | GSE222080 | GEO

Oncolytic virus M1 functions as a bi-functional checkpoint inhibitor to enhance the antitumor activity of DC vaccine

Project description:Oncolytic virus M1 functions as a bi-functional checkpoint inhibitor to enhance the antitumor activity of DC vaccine

| PRJNA917641 | ENA

Hepatocellular carcinoma specific epigenetic checkpoint bi-directionally regulates antitumor immunity of CD4+T cell

Project description:To investigate the effect of Matr3 CKO of CD4+ T cells on HCC of mice.

2024-05-29 | GSE263391 | GEO

A selective HDAC8 inhibitor potentiates antitumor immunity and efficacy of immune checkpoint blockade in hepatocellular carcinoma

Project description:A selective HDAC8 inhibitor potentiates antitumor immunity and efficacy of immune checkpoint blockade in hepatocellular carcinoma

| PRJNA690718 | ENA

Identification of a novel antitumor CD4+ T cell cluster orchestrating antitumor immunity

Project description:scRNAseq-based unsupervised clustering and clonotyping revealed that Th1/17 and CCR6 SP clusters formed metacluster Th7R, which was distinct from Th1 or Th17, characterized by high expression of the IL-7 receptor. Use of this cluster to assess antitumor CD4+ T cell immunity from the peripheral blood and to predict the efficacy of immune checkpoint inhibitors will pave the way for novel antitumor immunotherapy strategies for patients.

2022-12-21 | GSE168844 | GEO

A selective HDAC8 inhibitor potentiates antitumor immunity and efficacy of immune checkpoint blockade in hepatocellular carcinoma [ChIP-seq]

Project description:A selective HDAC8 inhibitor potentiates antitumor immunity and efficacy of immune checkpoint blockade in hepatocellular carcinoma [ChIP-seq]

| PRJNA690724 | ENA

A selective HDAC8 inhibitor potentiates antitumor immunity and efficacy of immune checkpoint blockade in hepatocellular carcinoma [RNA-seq]

Project description:A selective HDAC8 inhibitor potentiates antitumor immunity and efficacy of immune checkpoint blockade in hepatocellular carcinoma [RNA-seq]

| PRJNA690723 | ENA

Spermine Synthase Engages in Macrophages M2 polarization to Sabotage Antitumor Immunity in Hepatocellular Carcinoma

Project description:Disturbances in tumor cell metabolism reshape the tumor microenvironment (TME) and impair antitumor immunity, but the implicit mechanisms remain elusive. Here, we found that spermine synthase (SMS) was significantly upregulated in tumor cells, which correlated positively with immunosuppressive microenvironments and predicted poor survival in hepatocellular carcinoma (HCC) patients. Via “subcutaneous” and “orthotopic” HCC syngeneic mouse models and a series of in vitro coculture experiments, we identified elevated SMS level in HCC cells played a role in immune escape mainly through its metabolic product spermine, which induced tumor-associated macrophage (TAM) reprogramming and subsequently corresponded with a decreased antitumor functionality of CD8+ T cells. Mechanistically, we discovered that spermine reprogrammed TAM mainly by activating the PI3K-Akt-mTOR-S6K signaling pathway. Spermine inhibition in combination with immune checkpoint blockade effectively diminishes tumor burden in vivo. Our results expand the understanding of the critical role of metabolites in regulating cancer progression and anti-tumor immunity, and open new avenues for developing novel therapeutic strategies against HCC.

2024-11-11 | GSE277457 | GEO

Role of regorafenib in antitumor immunity in hepatocellular carcinoma

Project description:Role of regorafenib in antitumor immunity in hepatocellular carcinoma

| PRJNA626615 | ENA

cohesin spreads bi-directionally to form chromatin jets in C. elegans

Project description:cohesin spreads bi-directionally to form chromatin jets in C. elegans

| PRJNA996120 | ENA