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Hypoxia and inflammation induce synergistic transcriptome turnover in macrophages

ABSTRACT: Hypoxia and inflammation induce synergistic transcriptome turnover in macrophages

PROVIDER: PRJNA1029883 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26434953_1.fastq.gz	Fastqsanger.gz
	SRR26434953_2.fastq.gz	Fastqsanger.gz
	SRR26434954_1.fastq.gz	Fastqsanger.gz
	SRR26434954_2.fastq.gz	Fastqsanger.gz
	SRR26434955_1.fastq.gz	Fastqsanger.gz

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Hypoxia and inflammation induce synergistic transcriptome turnover in macrophages

Project description:Macrophages are effector immune cells that experience substantial changes to oxygenation when transiting through tissues, especially when entering tumors or infected wounds. How hypoxia alters gene expression and macrophage effector function at the post-transcriptional level remains poorly understood. Here we use TimeLapse-seq to measure how inflammatory activation modifies the hypoxic response in primary macrophages. Nucleoside recoding sequencing allows derivation of steady-state transcript levels, degradation rates, and transcriptional synthesis rates from the same dataset. We find that hypoxia produces distinct responses from resting and inflammatory macrophages. Hypoxia induces destabilization of mRNA transcripts, though inflammatory macrophages substantially increase mRNA degradation compared to resting macrophages. Increased RNA turnover results in upregulation of ribosomal protein genes and downregulation of extracellular matrix components in inflammatory macrophages. Hypoxia induces gene expression changes similar to tumorigenic macrophages in solid tumor biopsies, including increased ribosomal protein expression, implying that post-transcriptional control contributes to translation regulation in tumorigenic macrophages.

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Project description:Dynamic N6-methyladenosine (m6A) modification was previously identified as a ubiquitous post-transcriptional regulation that affected mRNA homeostasis. However, the m6A-related epitranscriptomic alterations and functions remain elusive in human diseases such as cancer. Here we show that hypoxia regulates the ‘reader’ protein YTH domain family 2 (YTHDF2), to eventually stabilize the methylated oncogene mRNAs in inflammation-associated liver cancer. YTHDF2 silenced in human cancer cells or depleted in mouse hepatocytes evoked pro-inflammatory responses and accelerated tumor growth and metastatic progression. Under hypoxia, YTHDF2 processed the decay of m6A-containing interleukin 11 (IL11) and serpin family E member 2 (SERPINE2) mRNAs, which were responsible for the inflammation-mediated malignancy. Reciprocally, YTHDF2 transcription succumbed to hypoxia-inducible factor-2α (HIF-2α). Administration of a HIF-2α antagonist (PT2385) restored YTHDF2-programed epigenetic machinery and repressed liver cancer. Hence, our findings provide a new insight into the mechanism by which hypoxia adapts m6A-mRNA editing to promote cancer.

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