Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA246458 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1275500.fastq.gz | Fastqsanger.gz | |||
| SRR1275501.fastq.gz | Fastqsanger.gz | |||
| SRR1275502.fastq.gz | Fastqsanger.gz | |||
| SRR1275503.fastq.gz | Fastqsanger.gz | |||
| SRR1275504.fastq.gz | Fastqsanger.gz |
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Project description:HEXIM1 is induced by DHODH inhibition to suppress melanoma
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Project description:Recent evidence suggests that leflunomide, a DHODH inhibitor, disrupts neural crest development and melanoma pathogenesis via inhibiting transcription elongation. Here, we provide evidence that a transcriptional regulator, HEXIM1, is upregulated in response to leflunomide. HEXIM1 is assembled into the 7SK snRNP complex to sequester and inhibit the kinase P-TEFb. P-TEFb triggers elongation by phosphorylating RNA polymerase II and pausing factors. Knockdown of hexim in zebrafish rescues the effects of leflunomide. HEXIM1 expression is low in human melanoma. In addition, HEXIM1 overexpression can suppress melanoma onset in zebrafish. Increased HEXIM1 expression, in response to low nucleotides triggered by DHODH inhibition, sequesters P-TEFb away from melanoma pathogenesis, proliferation and cell cycle genes based on GRO-seq and ChIP-seq analyses. This reduces productive elongation at genes that maintain the tumorigenic state. Our study illustrates that HEXIM1 is a tumor suppressor that responds to cell stress, consequently inhibiting productive elongation of proliferative genes in melanoma.
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Project description:Nucleotide stress induction of HEXIM1 suppresses melanoma by modulating cancer cell-specific gene transcription [ChIP-Seq]
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Project description:Cancer metabolism has been actively studied to gain insights into tumorigenic survival mechanisms and susceptibilities. In melanoma, we identify HEXIM1, a transcription elongation regulator, as a novel melanoma suppressor that participates in nucleotide stress regulation. HEXIM1 expression is low in melanoma. Its overexpression suppresses melanoma while its inactivation accelerates tumor onset in vivo. HEXIM1 responds to nucleotide stress. Knockdown of HEXIM1 rescues neural crest and melanoma nucleotide stress phenotypes in vivo. Mechanistically, under nucleotide stress, HEXIM1 is induced to form an inhibitory complex with P-TEFb, the kinase that initiates transcription elongation, to pause transcription at tumorigenic genes. The resulting alteration in gene expression also causes anti-tumorigenic transcripts to bind to and be stabilized by HEXIM1. HEXIM1 therefore plays an important role in inhibiting cancer cell-specific gene transcription while also facilitating anti-cancer gene expression. Our study reveals a novel role for HEXIM1 in coupling nucleotide metabolism with transcriptional regulation in melanoma.
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Project description:Cancer metabolism has been actively studied to gain insights into tumorigenic survival mechanisms and susceptibilities. In melanoma, we identify HEXIM1, a transcription elongation regulator, as a novel melanoma suppressor that participates in nucleotide stress regulation. HEXIM1 expression is low in melanoma. Its overexpression suppresses melanoma while its inactivation accelerates tumor onset in vivo. HEXIM1 responds to nucleotide stress. Knockdown of HEXIM1 rescues neural crest and melanoma nucleotide stress phenotypes in vivo. Mechanistically, under nucleotide stress, HEXIM1 is induced to form an inhibitory complex with P-TEFb, the kinase that initiates transcription elongation, to pause transcription at tumorigenic genes. The resulting alteration in gene expression also causes anti-tumorigenic transcripts to bind to and be stabilized by HEXIM1. HEXIM1 therefore plays an important role in inhibiting cancer cell-specific gene transcription while also facilitating anti-cancer gene expression. Our study reveals a novel role for HEXIM1 in coupling nucleotide metabolism with transcriptional regulation in melanoma.
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Project description:Cancer metabolism has been actively studied to gain insights into tumorigenic survival mechanisms and susceptibilities. In melanoma, we identify HEXIM1, a transcription elongation regulator, as a novel melanoma suppressor that participates in nucleotide stress regulation. HEXIM1 expression is low in melanoma. Its overexpression suppresses melanoma while its inactivation accelerates tumor onset in vivo. HEXIM1 responds to nucleotide stress. Knockdown of HEXIM1 rescues neural crest and melanoma nucleotide stress phenotypes in vivo. Mechanistically, under nucleotide stress, HEXIM1 is induced to form an inhibitory complex with P-TEFb, the kinase that initiates transcription elongation, to pause transcription at tumorigenic genes. The resulting alteration in gene expression also causes anti-tumorigenic transcripts to bind to and be stabilized by HEXIM1. HEXIM1 therefore plays an important role in inhibiting cancer cell-specific gene transcription while also facilitating anti-cancer gene expression. Our study reveals a novel role for HEXIM1 in coupling nucleotide metabolism with transcriptional regulation in melanoma.
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