Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1106924 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28868138_1.fastq.gz | Fastqsanger.gz | |||
| SRR28868138_2.fastq.gz | Fastqsanger.gz | |||
| SRR28868139_1.fastq.gz | Fastqsanger.gz | |||
| SRR28868139_2.fastq.gz | Fastqsanger.gz | |||
| SRR28868140_1.fastq.gz | Fastqsanger.gz |
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Project description:Urothelial carcinoma of the bladder, the second most prevalent cancer within the urothelial system, often evades immune recognition by natural killer (NK) cells, but studies have shown that cyproheptadine (CPH), an anti-histamine drug, exhibits anticancer effects in this carcinoma. Co-culturing CPH-treated cells with NKG2D-expressing NK92 cells resulted in enhanced NK-mediated lysis of UC cells, with RNA-seq analysis revealing increased expression of the NKG2D ligand ULBP2 in CPH-treated cells. We hypothesize that cyproheptadine as a epigenetic modifier enhances NK-mediated cytotoxicity by restoring NKG2D ligands and CCL3 and as a control we used entinostat a known FDA approved HDAC1/3 inhibitor. Targeting NK cells offers a promising strategy against urothelial carcinoma. Further analysis showed epigenetic regulation of ULBP2 expression with increased H3K27Ac active mark enrichment in CPH-treated cells. Overexpression of ULBP2 led to increased NK-mediated lysis, while knockdown reduced it in CPH-treated urothelial carcinoma cells. Additionally, CPH treatment enhanced the anti-tumor effect in a mouse model, likely due to increased NK and NKT cell infiltration. In summary, CPH triggers an innate immune response against urothelial carcinoma by promoting NK cell-mediated cytotoxicity through ULBP2 and CCL3 restoration.
2025-06-24 | GSE266660 | GEO
Project description:Radiation and BCG instillations are used clinically for treatment of urothelial carcinoma, but the precise mechanisms by which they activate an immune response remain elusive. The role of the cGAS-STING pathway has been implicated in both BCG and radiation-induced immune response however comparison of STING-pathway molecules and immune landscape following treatment in urothelial carcinoma has not be performed. We therefore comprehensively analyzed the local immune response in the bladder tumor microenvironment following radiotherapy and BCG instillations in a well-established spontaneous murine model of urothelial carcinoma to provide insight into activation of STING-mediated immune response. Mice were exposed to the oral carcinogen, BBN, for 12 weeks prior to treatment with a single 15Gy dose of radiation or 3 intravesical instillations of BCG (1x108 CFU). At sacrifice, tumors were staged by a urologic pathologist and effects of therapy on the immune microenvironment were measured using NanoString Myeloid Innate Immunity Panel and immunohistochemistry. Clinical relevance was established by measuring immune biomarker expression of cGAS and STING on a human tissue microarray consisting of BCG-treated non-muscle invasive urothelial carcinomas. BCG instillations in the murine model elevated STING and downstream STING-induced interferon and pro-inflammatory molecules, intratumoral M1 macrophage and T-cell accumulation, and complete tumor eradication. In contrast, radiotherapy caused no changes in STING pathway or innate immune gene expression; rather, it induced M2 macrophage accumulation and elevated FoxP3 expression characteristic of immunosuppression. In human non-muscle invasive bladder cancer, STING protein expression was elevated at baseline in patients who responded to BCG therapy and increased further after BCG therapy. Overall, these results show that STING pathway activation plays a key role in effective BCG-induced immune response and strongly indicate that the effects of BCG on the bladder cancer immune microenvironment are more beneficial than those induced by radiation.
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Project description:Smoking is a major risk factor for Urothelial carcinoma (UC). However the complex mechanisms, how smoking promotes carcinogenesis and tumour progression, remain obscure. A microarray based approached was therefore performed to detect the smoking derived gene expression alteration in non-malignant and malignant urothelial tissues from patients with superficial or invasive UC. Smoking enhanced cell migration and response to tissue damages. In non-malignant tissues smoking induced immune response and altered the cytoskeleton. In urothelial carcinoma, smoking altered extracellular and chromosome structures. Smoking affected tissues from patients with invasive carcinomamore strongly, up-regulating particularly growth factors and oncogenes in non-malignant tissue of patients with invasive but not with superficial carcinoma. In former smokers, comparable changes were seen in tissues form patients with invasive disease while they were minor or reversed in tissue of patients with superficial disease. Best but not complete tissue repair was suggestedfor non-malignant tissue from patients with superficial tumours. we used microarray techniques to define gene expression profile which may explain the contribution of smoking to urothelial carcinoma. Gene expression profiling using GeneChip HG-U133A Plus 2.0 (Affymetrix) was performed on non-malignant and carcinogenic urothelium from six patients with superficial and six with invasive urothelial carcinoma, each group including two current, former, and non-smokers.
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Project description:Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [ATAC-Seq]
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Project description:Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [ChIP-Seq]
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Project description:Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [RNA-Seq]
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Project description:The Phase 3 1L urothelial carcinoma (IMvigor130) trial revealed more favorable effects on overall survival with atezolizumab combined with gemcitabine and cisplatin (GemCis) than with atezolizumab combined with gemcitabine and carboplatin (GemCarbo). This study investigates the immunomodulatory effects of cisplatin vs carboplatin as a potential explanation for these clinical observations. GemCis compared with GemCarbo ± atezolizumab induced transcriptional changes in circulating immune cells, including upregulation of antigen presentation and T-cell activation programs. In vitro experiments demonstrated that cisplatin, compared with carboplatin, exerted direct immunomodulatory effects on cancer cells, promoting dendritic cell activation and antigen-specific T cell killing. These results underscore the key role of immune modulation in cisplatin's efficacy in urothelial carcinoma and highlight the potential importance of specific chemotherapy backbones for immune checkpoint blockade combination therapies.
2023-11-02 | GSE235066 | GEO
Project description:We sought for new treatment strategies to improve response of urothelial carcinoma (UC) patients towards immune therapy. Epigenetic inhibitors may modulate expression of immune response regulators and alter the immune phenotype of UC cells. Thus, we determined whether longterm pretreatment of UC cell lines with the DNMT inhibitor decitabine (DEC) at low dosemight enhance killing by CAR-T cells. We engineered target-specific CAR-T cells recognizing EGFR and CD44v6 on UCC. To define underlying mechanisms we performed RNA Seq analysis for two UC cell lines treated accordingly.
2021-12-08 | GSE164862 | GEO
Project description:Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 1]
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