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Citrullination modulation maintains HIF-1A stabilization to drive tumor progression

ABSTRACT: Citrullination modulation maintains HIF-1A stabilization to drive tumor progression

PROVIDER: PRJNA977946 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24771160_1.fastq.gz	Fastqsanger.gz
	SRR24771160_2.fastq.gz	Fastqsanger.gz
	SRR24771161_1.fastq.gz	Fastqsanger.gz
	SRR24771161_2.fastq.gz	Fastqsanger.gz
	SRR24771162_1.fastq.gz	Fastqsanger.gz

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Citrullination modulation maintains HIF-1A stabilization to drive tumor progression

Project description:HIF-1 (Hypoxia-inducible factor 1) is the master regulator responding to hypoxic conditions. Here, we found that HIF-1A is citrullinated by peptidyl arginine deiminase 4 (PADI4) at arginine 698, promoting HIF-1A stabilization and thus HIF-1-driven tumor growth. The knockdown of PADI4 could dramatically decrease HIF-1 protein expression without affecting the mRNA level, and this could be rescued by the proteasome inhibitor MG132 treatment under hypoxia. And PADI4-HIF-1A interaction is critical for HIF-1A stability and tumor progression, depending on the enzymatic activity of PADI4 and the pocket structure of PADI4. DHE, an FDA-approved agent for the treatment of migraine, was found serve as a potential antitumor agent throgh disrupting PADI4-HIF-1A interaction and suppressing HIF-1A stability. Taken together, we found the anti-tumor effect of DHE due to its effect on blocking PADI4-HIF-1A interaction and downregulating HIF-1A pathway in cancer cells. To figure out the influence of DHE on liver cancer cell under hypoxia, we treated Hep3B cell lines with two does DHE in 6 hours under Hypoxia and extracted mRNA for furthur RNA seq.

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mesendoderm differentiation with Hif-1a knockdown

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Defective mitochondrial cardiolipin remodeling dampens HIF-1a expression in hypoxia

Project description:Mitochondria fulfill vital metabolic functions and act as crucial cellular signaling hubs integrating their metabolic status into the cellular context. Here, we show that defective cardiolipin-remodeling, upon loss of the cardiolipin acyl transferase Tafazzin, mutes HIF-1a signaling in hypoxia. Tafazzin-deficiency does not affect posttranslational HIF-1a regulation but rather HIF-1a gene-expression, a dysfunction recapitulated in iPSCs-derived cardiomyocytes from Barth Syndrome patients with Tafazzin-deficiency. RNAseq analyses confirmed drastically altered signaling in Tafazzin mutant cells. In hypoxia, Tafazzin-deficient cells display reduced production of reactive oxygen species (ROS) perturbing NF-kB activation and concomitantly HIF-1a gene-expression. In agreement, Tafazzin-deficient mice hearts display reduced HIF-1a levels and undergo maladaptive hypertrophy with heart failure in response to pressure overload challenge. We conclude that defective mitochondrial cardiolipin-remodeling dampens HIF-1a signaling through inactivation of a non-canonical signaling pathway: Lack of NF-kB activation through reduced mitochondrial ROS production diminishes HIF-1a transcription.

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mesendoderm differentiation with Hif-1a knockdown

Project description:mesendoderm differentiation with Hif-1a knockdown

| PRJNA826451 | ENA