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ZNF207 promotes hepatocellular carcinoma by reprogramming kynurenine metabolism and inhibiting CD8+ T cell infiltration

ABSTRACT: ZNF207 promotes hepatocellular carcinoma by reprogramming kynurenine metabolism and inhibiting CD8+ T cell infiltration

PROVIDER: PRJNA705607 | ENA |

REPOSITORIES: ENA

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ZNF207 promotes hepatocellular carcinoma by reprogramming kynurenine metabolism and inhibiting CD8+ T cell infiltration

Project description:Bioinformatic analysis identified ZNF207 as an immunosuppressive molecule in HCC. P53R249S mutation and hypoxia synergistically elevated ZNF207 expression. Silencing ZNF207 affected tumor growth in normal mice, but not in immunodeficient mice. Flow cytometry analysis showed increased proportion of CD8+ T cells in tumor tissues while exhaustion decreased after knocking down ZNF207. Mechanism studies showed that CX3CL1 was involved in the chemotaxis of CD8+ T cells, and ZNF207 regulated kynurenine production through transcriptional regulation of IDO1, then promoting the exhaustion of CD8+ T cells. High expression of ZNF207 showed a lower response rate to immunotherapy. In vivo experiments also confirmed the efficacy of ZNF207 knockdown combined with PD1 monoclonal antibody was better than PD1 alone.

2022-03-16 | GSE167935 | GEO

Gene expression profile of hepatocellular carcinoma with marked immune cell infiltration II

Project description:Gene expression profile of hepatocellular carcinoma with marked immune cell infiltration II

| PRJNA513314 | ENA

Gene expression profile of hepatocellular carcinoma with marked immune cell infiltration I

Project description:Gene expression profile of hepatocellular carcinoma with marked immune cell infiltration I

| PRJNA513315 | ENA

The aryl hydrocarbon receptor binds to kynurenine and mediates a signal supports the undifferentiated state in pluripotent stem cells

Project description:Kynurenine is generated from tryptophan by indoleamine 2,3-dioxygenase (IDO1) and binds to the aryl hydrocarbon receptor (AhR). We found that kynurenine generated by human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs) stimulated the AhR to bind selectively to the promoters and enhancers of self-renewal genes, thus enhancing their transcription. The kynurenine-AhR complex also directly stimulated the expression of IDO1 and AHR, activating a positive feedback loop. Substantial amounts of kynurenine that were not complexed with AhR were present in the culture medium, providing a paracrine signal for maintenance of the undifferentiated state. Kynurenine was not present in the medium of differentiated ESCs and iPSCs. When cells were induced to undergo ectodermal differentiation, the abundance of kynurenine in the medium was reduced through activation of the main kynurenine catabolic pathway mediated by aminotransferase 2 (KAT2), resulting in the secretion of 2-aminoadipic acid (2-AAA) into the culture medium. Thus, kynurenine in the culture medium is a biomarker for the undifferentiated state, and 2-AAA in the culture medium is a biomarker for ESCs and iPSCs that have committed to differentiate along the ectoderm lineage.

2019-06-09 | GSE129507 | GEO

Gene expression profile of hepatocellular carcinoma with marked immune cell infiltration I

Project description:Tumor microenvironmental characteristics using gene expression profiles in hepatocellular carcinoma with marked immune stroma (HCC-IS) compared to conventional hepatocellular carcinoma (C-HCC).

2019-06-07 | GSE124751 | GEO

Gene expression profile of hepatocellular carcinoma with marked immune cell infiltration II

2019-06-07 | GSE124752 | GEO

WISP2/CCN5 is a prognostic biomarker influenced by tumour purity and fibroblast infiltration in hepatocellular carcinoma

Project description:Background Hepatocellular carcinoma (HCC) is the second leading cause of cancer death worldwide. The dismal outcome is attributable to high frequency of recurrence and metastasis. Therefore, identification of effective biomarkers is a key strategy to inform prognosis and improve survival of HCC patients Methods We analysed expression of WNT-1-induced signalling protein-2 (WISP2) and the prognostic correlation in HCC patients using Oncomine, Kaplan Meier plotter, and Gene Expression Profiling Interactive Analysis 2 (GEPIA2) . We explored the role of WISP2 in HCC using the Cancer Cell Line Encyclopedia (CCLE) and gene microarrays and then assessed the correlation between WISP2 and stromal cells in tumour tissues using the Tumor IMmune Estimation Resource (TIMER). Finally, the role of WISP2 and its relationship with tumour purity and fibroblast infiltration were examined both in vitro and in vivo. Results WISP2 was downregulated in HCC tissues, and high expression of WISP2 was associated with better prognosis in patients with certain clinicopathologic characteristics. Upregulation of WISP2 in HCC was related to inhibition of the malignant phenotype in vitro, but these alterations were not observed in vivo . WISP2 also negatively correlated with tumour purity, and increased infiltration of fibroblasts promoted malignant progression in HCC tissues. The enhanced infiltration ability of fibroblasts was related to upregulated high-mobility group protein 1 (HMGB1) after overexpression of WISP2 in HCC. Conclusions The findings shed light on the anticancer role of WISP2 in HCC, suggest that WISP2 overexpression may serve as a biomarker for better prognosis, and indicate that WISP2 expression is influenced by tumour purity and fibroblast infiltration.

2019-07-20 | GSE134563 | GEO

Kynurenine treatment of herpesivrus stimulated iCD103 dendritic cells

Project description:We report the gene expression (obtained by next generation RNAseq) of inducible CD103+ dendritic cells, iCD103 cells, stimulated with both murine herpesvirus-68 and the immunomodulatory tryptophan derivative kynurenine (kyn). This study provides data on how tryptophan derivatives can modulate pro-inflammatory cytokine expression in virus treated dendritic cells.

2021-01-01 | GSE160307 | GEO

Luteolin exerts anti-tumor immunity in hepatocellular carcinoma by accelerating CD8+ T lymphocyte infiltration

Project description:We observed that luteolin effectively restrained the growth of solid tumors in the established mouse model of HCC. Expression spectrum chip sequencing showed that treatment with luteolin could promote T cell activation, cell chemotaxis and cytokine production. Furthermore, we explored the influence of luteoin on the phenotypic and functional alterations of T cells. Our findings revealed that luteolin maintained a high ratio of CD8+ T cells in the peripheral blood, spleen, and tumor tissues. Additionally, luteolin restored the cytotoxicity of tumor-infiltrating CD8+ T cells in H22 tumor-bearing mice. Moreover, CD8+ T cells showed stronger activation phenotypes and more production of IFN-γ, TNFα, and Granzyme B in serum. Furthermore, the co-administration of luteolin and PD-1 mAb resulted in potentiated anti-tumor effects in H22 tumor-bearing mice.These findings indicate that luteolin could exert an anti-tumor immune response by inducing CD8+ T cell infiltration and enhance the anti-tumor effects of PD-1 mAb in HCC treatment in H22 tumor-bearing mice.

2023-09-20 | GSE243341 | GEO

MED12 mutation activates the tryptophan/kynurenine/AHR pathway to promote growth of uterine leiomyomas

Project description:Uterine leiomyoma (LM) is the most common tumor in women. Estrogen and progesterone, via their receptors ERα and PR, play essential roles in LM growth. Mediator complex subunit 12 (MED12) mutations occur in 70% of all LM and are thought to drive tumor growth in a steroid hormone-dependent manner; however, the mechanisms remain unclear. Here, we performed ChIP-seq (ERα, PR, and MED12) and RNA-seq on LM expressing mutant MED12 (mut-MED12) or wild-type MED12 and matched myometrium. Mut-MED12 altered PR and chromatin interaction landscapes, with significant PR-binding site loss in proximal promoter regions in mut-MED12 LM. Integration of cistrome and transcriptome data identified tryptophan 2,3-dioxygenase (TDO2) as a PR and MED12 target gene, which was aberrantly upregulated in mut-MED12 LM. Kynurenine, the catabolic product of TDO2, was significantly elevated in mut-MED12 LM. Tryptophan or kynurenine treatment of primary LM cells activated the aryl hydrocarbon receptor (AHR) pathway, increased cell proliferation, and inhibited apoptosis; blocking the TDO2-kynurenine-AHR pathway by siRNA knockdown or pharmacologic inhibition abolished these effects. Mut-MED12 LM cells showed higher sensitivity to these treatments. These findings suggest that activation of the TDO2-kynurenine-AHR pathway in mut-MED12 LM induces tumor growth, and may inform the development of targeted treatments and precision medicine in LM.

2023-05-01 | GSE204968 | GEO

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