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The Dual Role of CREPT in Glioblastoma: Promoting Proliferation and Shaping an Immunosuppressive Microenvironment through Chemo-MO and GZMK⁺ T Cell Interaction

ABSTRACT: The Dual Role of CREPT in Glioblastoma: Promoting Proliferation and Shaping an Immunosuppressive Microenvironment through Chemo-MO and GZMK⁺ T Cell Interaction

PROVIDER: PRJNA1299322 | ENA |

REPOSITORIES: ENA

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The Dual Role of CREPT in Glioblastoma: Promoting Proliferation and Shaping an Immunosuppressive Microenvironment through Chemo-MO and GZMK⁺ T Cell Interaction

Project description:Elevated CREPT promotes tumor cell proliferation and enhances CCL2 secretion, thereby recruiting Chemo-MOs. These Chemo-MOs then engage in regulatory interactions with GZMK+CD8+ T cells, suppressing T cell infiltration and ultimately establishing a robust immunosuppressive microenvironment.

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ChIP-seq of CREPT in intestinal crypts

Project description:CREPT was demonstrated as a key regulator of intestinal stem cells. To figure out the role of CREPT on transcription level, a ChIP-seq experiment was performed to identify the CREPT down-stream genes in intestinal crypt cells.

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Microenvironment-induced CREPT expression by cancer-derived small extracellular vesicles primes field cancerization

Project description:Cancer local recurrence increases the mortality of patients, and might be caused by field cancerization, a pre-malignant alteration of normal epithelial cells. It has been suggested that cancer-derived small extracellular vesicles (CDEs) may contribute to field cancerization, but the underlying mechanisms remain poorly understood. In this study, we aim to identify the key regulatory factors within recipient cells under the instigation of CDEs. In vitro experiments were performed to demonstrate that CDEs promote the expression of CREPT in normal epithelial cells. TMT-based quantitative mass spectrometry was employed to investigate the proteomic differences between normal cells and tumor cells. Loss-of-function approaches by CRISPR-Cas9 system were used to assess the role of CREPT in CDEs-induced field cancerization. RNA-seq was performed to explore the genes regulated by CREPT during field cancerization. CDEs promote field cancerization by inducing the expression of CREPT in non-malignant epithelial cells through activating the ERK signaling pathway. Intriguingly, CDEs failed to induce field cancerization when CREPT was deleted, highlighting the importance of CREPT. Transcriptomic analyses revealed that CDEs elicited inflammatory responses, primarily through activation of the TNF signaling pathway. CREPT, in turn, regulates the transduction of downstream signals of TNF by modulating the expression of TNFR2 and PI3K, thereby promoting inflammation-to-cancer transition. CREPT not only serves as a biomarker for field cancerization, but also emerges as a target for preventing the cancer local recurrence.

2023-12-10 | GSE249383 | GEO

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SMN MO, Gemin2 MO knockdown vs Control MO injected

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Zebrafish embryos: Control MO vs. Lin28A MO vs. Lin28B MO injected

Project description:miRNA profiling of zebrafish embryos comparing control MO with Lin28A MO or Lin28B MO injected embryos at 5hpf

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