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Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion

ABSTRACT: Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion

PROVIDER: PRJNA883199 | ENA |

REPOSITORIES: ENA

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Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion [scRNAseq]

Project description:Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion [scRNAseq]

| PRJNA883203 | ENA

Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion [bulkRNAseq]

Project description:Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion [bulkRNAseq]

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Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion [scRNAseq]

Project description:Accumulated genetic mutations or copy number alterations are frequently observed in esophageal squamous cell carcinoma (ESCC) patients. However, it is still elusive which gene is the driver to initiate ESCC. We identified key genetic determinants for ESCC development using CRISPR/Cas9-based multiple genes KO mouse esophageal organoid model. Trp53, Cdkn2a, and Notch1 triple KO (PCN) organoid showed the phenotypes of ESCC. These triple genes KO served for cell proliferation through building multiple root cell clusters and remodeling the immune landscape beneficial for tumorigenesis by Ccl2-Ccr2 mediated intercellular interactions. Ccl2-releasing PCN tumors were surrounded by exhausted T cells and M2 macrophages leading to immune evasion. The PCN-type tumor was observed in more than 30% of ESCC patients who express high levels of B2M, CCL2, and NF-kB. Our study unveiled genetic determinants for ESCC development crucial for cell-autonomous growth as well as non-cell autonomous interactions with immune cells.

2023-06-07 | GSE213927 | GEO

Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion [bulkRNAseq]

2023-06-07 | GSE213904 | GEO

Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-07 | GSE213929 | GEO

Molecular Determinants of Esophageal Cancer in Tanzania

Project description:Molecular Determinants of Esophageal Cancer in Tanzania

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Molecular Determinants of Esophageal Cancer in Tanzania

Project description:Molecular Determinants of Esophageal Cancer in Tanzania

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Human esophageal dysplasia (16 cases) vs. esophageal squamous cell carcinoma (59 cases)

Project description:Our aim is to identify frequent genomic aberrations both in ESCC and esophageal dysplasia, and to discover important copy number-driving genes and microRNAs in ESCC. We carried out array-based comparative genomic hybridization (array CGH) on 59 ESCC resection samples and 16 dysplasia biopsy samples. Expression of genes at 11q13.3 was analyzed by real-time PCR and immunohistochemistry (IHC). Integrated analysis was performed to identify genes or microRNAs with copy number-expression correlations. Two group experiment, esophageal dysplasia vs. esophageal squamous cell carcinoma. Biological replicates: 16 dysplasias vs. 59 carcinomas

2013-04-29 | E-GEOD-46452 | biostudies-arrayexpress

METTL3 mediated m6A mRNA modification promotes esophageal cancer initiation and progression via Notch signaling pathway

Project description:Esophageal cancer is a lethal malignancy with high mortality rate, while the molecular mechanisms underlying esophageal cancer pathogenesis are stillis poorly understood. Here we found that the N6-methyladenosine (m6A) methyltransferase METTL3 is significantly up-regulated in esophageal squamous cell carcinoma (ESCC) and associated with poor patient prognosis. Depletion of METTL3 results in decreased ESCC growth and progression in vitro and in vivo. We further established ESCC initiation and progression models using Mettl3 conditional knockout mouse and revealed that Mettl3 mediated m6A modification is essential for promotes ESCC initiation and progression in vivo. Moreover, using METTL3 overexpression ESCC cell model and Mettl3 conditional knockin mouse model, we demonstrated the critical function of Mettl3 in promoting in vivo ESCC tumorigenesis in vitro and in vivo. Mechanistically, Mettl3 catalyzed m6A modification promotes NOTCH1 expression and the activation of Notch signaling pathway. Forced activation of Notch signaling pathway successfully rescues the growth, migration and invasion capacities of METTL3 depleted ESCC cells. Our data uncovered important mechanistical insights underlying ESCC tumorigenesis and provided molecular basis for the development of novel strategies for ESCC diagnosis and treatment.

2021-09-15 | GSE179267 | GEO

Identification of sequence-specific promoters driving polycistronic transcription initiation by RNA Polymerase II in trypanosomes

Project description:Protein coding genes in the trypanosome genome are organized in polycistronic transcription units (PTUs). How RNA Polymerase II (Pol II) initiates PTU transcription has not been resolved and the current model favors initiation driven by chromatin epigenetic marks, rather than core-promoters. Here, we identify sequence-specific core promoters by functional characterization of ChIP-Seq Pol II accumulation-peaks. Sequences located between oppositely orientated PTUs contained two independent and distinct core promoters, driving unidirectional transcription. Detailed analysis of one promoter identified 75 bp, necessary and sufficient to fully drive reporter expression, and containing short functional motifs. Analysis of further promoters suggested activity and initiation is regulated and both, focused and dispersed transcription patterns were found. Thus, in contrast to the model of unregulated and promoter-independent transcription initiation, sequence-specific promoters determine the initiation of RNA Pol II transcription of protein coding genes in trypanosomes. These findings resolve the discrepancy between trypanosomes and other eukaryotes in how Pol II initiates protein-coding gene transcription.

2021-02-01 | GSE130798 | GEO

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