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CMTR1 is recruited to transcription start sites and has enhanced influence over ribosomal protein and histone genes [ChIP-seq]

ABSTRACT: We investigated the gene-specificity of mRNA cap methyltransferase CMTR1 and its impact in RNA expression. In this ChIP-seq experiment, we investigated the genome-wide chromatin binding profiles of CMTR1 in mouse embryonic stem cells. We demontrated that CMTR1 binds to the transcription start site (TSS) correlating with RNA polymerase II (RNAP II) levels, with predominant binding at histone genes and ribosomal protein (RP) genes. Moreover, the repression of CMTR1 expression resulted in a loss of RNAP II binding at the TSS.

ORGANISM(S): Mus musculus

PROVIDER: GSE175628 | GEO | 2022/02/25

REPOSITORIES: GEO

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CMTR1 is recruited to transcription start sites and has enhanced influence over ribosomal protein and histone genes [RNA-seq]

Project description:We investigated the gene-specificity of mRNA cap methyltransferase CMTR1 and its impact in RNA expression. In this RNA-seq experiment, we used siRNA to knockdown the endogenous CMTR1 protein to investigate its role in mouse embryonic stem cells. We demonstrated that the repression of CMTR1 expression resulted in a loss of RNA expression, particularly of histone and ribosomal protein genes.

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Project description:CMTR1, also called IFN-stimulated gene 95 kDa protein (ISG95), is elevated by viral infection in a variety of cells. However, the function of CMTR1 in colorectal cancer (CRC), especially its role in tumorigenesis and immune regulation, remains unclear. Here, we first identified CMTR1 as a novel oncogene in colorectal cancer. Based on The Cancer Genome Atlas (TCGA) database exploration and human tissue microarray (TMA) analysis, we found that CMTR1 expression was markedly higher in colorectal cancer tissues compared to that in adjacent normal tissues. High CMTR1 was correlated with poor prognosis of colorectal cancer patients. Knockdown (KD) of CMTR1 significantly suppressed cell proliferation and tumorigenicity both in vitro and in vivo, whereas overexpression of CMTR1 exhibited the opposite effects. KEGG analysis revealed that the JAK/STAT signaling pathway was differentially enriched in colorectal cancer cells with CMTR1 KD. Mechanistically, repression of CMTR1 influenced RNAPII recruitment to the TSS and repression of STAT3 expression and activation. Furthermore, PD1 blockade immunotherapy was prominently enhanced with CMTR1 KD by increased infiltration of CD8+ T cells into tumor microenvironment. Overall, it appears that CMTR1 plays a key role in regulating tumor cell proliferation and antitumor immunity.

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