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Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC

ABSTRACT: Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC

PROVIDER: PRJNA909221 | ENA |

REPOSITORIES: ENA

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Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC (RIP-Seq)

Project description:Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC (RIP-Seq)

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Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC (RIP-Seq)

Project description:Ac4C-binding RNAs were analyzed by imprinting RNA-sequencing of anti-Ac4C antibody-retrieved complexes from macrophages lysate. We then performed gene expression profiling analysis using data obtained from RIP-seq of peritoneal macrophages incubated with IFN-G

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Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC

Project description:To investigated how NAT10 inhibitor (Remodelin hydrobromide) affected the function of peritoneal macrophages , we treated peritoneal macrophages IFN y，Remodelin hydrobromide and Remodelin hydrobromide with IFN y. We then performed gene expression profiling analysis using data obtained from RNA-seq of peritoneal macrophages with four treaments

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chemical ac4C sequencing (ac4C-seq) to identify mRNA ac4C sites

Project description:NAT10-catalyzed N4-acetylcytidine (ac4C) has emerged as a vital post-transcriptional modulator on the coding transcriptome by promoting mRNA stability. To explore the transcriptome-wide profile of ac4C modification, we mapped the locations of ac4C modification on wild-type (WT) hESCs and NAT10 KD hESCs by NaCNBH3-based chemical ac4C sequencing (ac4C-seq).

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chemical ac4C sequencing (ac4C-seq) to identify mRNA ac4C sites

Project description:chemical ac4C sequencing (ac4C-seq) to identify mRNA ac4C sites

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Identification of proteins specifically binding to ac4C RNA probes

Project description:As a newly identified mRNA modification, the regulation of ac4C remains largely unexplored. RNA-binding proteins (RBPs) that specifically binds to ac4C modification and mediate downstream cellular activities (readers) have not been reported yet. We synthesized acetylated and non-acetylated RNA probes by in vitro transcription. The sequences of the probes were segments of FUS and 18s rRNA, which contain ac4C sites as reported. A biotin-RNA pulldown assay and mass spectrometry were performed with HEK 293T cell lysates.

2021-07-20 | PXD027014 | Pride

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Comparison of metastasis-inclined microenvironment (MIM) and metastasis-averse microenvironment (MAM) HCC patients

Project description:To determine the role of the hepatic microenvironment in HCC metastasis, we compared the gene expression profiles of 20 noncancerous surrounding hepatic tissues from two HCC patient groups, those with primary HCC together with venous metastasis which we termed a metastasis-inclined microenvironment (MIM) and those with HCC without detectable metastasis, which we termed a metastasis-averse microenvironment (MAM). There were a total of 20 cDNA microarrays performed, comparing 9 MIM or 11 MAM HCC patient samples to a common reference pool of 8 normal liver tissues.

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Effect of knock-down of circASH2 on gene expression in HCC cells

Project description:Metastasis, especially intrahepatical, is a major challenge for hepatocellular carcinoma (HCC) treatment. Cytoskeleton remodeling has been identified as a vital process mediating intrahepatic spreading. Previously we reported HCC tumor adhesion and invasion were modulated by circular RNA (circRNA), which has emerged as important regulators of various cellular processes and has been implicated in the cancer progression. Here we uncovered a novel nuclear circRNA, circASH2, which is preferentially lost in HCC tissues, and inhibits HCC metastasis by altering tumor cytoskeleton structure. Tropomyosin 4 (TPM4), a critical binding protein of actin, turned out to be the major target of circASH2 and was post-transcriptionally suppressed. Such regulation is based on mRNA/pre-mRNA splicing and degradation process. Furthermore, liquid-liquid phase separation (LLPS) of nuclear Y-box binding protein 1 (YBX1) enhanced by circASH2 augments TPM4 transcripts decay. Together, our data have revealed a novel tumor suppressive circRNA and more importantly, uncovered a fine regulation mechanism for HCC progression.

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