Transcriptome analysis after ALKBH3 knockdown in ocular melanoma cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA882062 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21627318_1.fastq.gz | Fastqsanger.gz | |||
| SRR21627318_2.fastq.gz | Fastqsanger.gz | |||
| SRR21627319_1.fastq.gz | Fastqsanger.gz | |||
| SRR21627319_2.fastq.gz | Fastqsanger.gz | |||
| SRR21627320_1.fastq.gz | Fastqsanger.gz |
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Project description:To study the mechanism of ALKBH3 in ocular melanoma, we performed RNA-seq of wide type cells and ALKBH3-deficient cells.
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Project description:Background: The oxidative DNA demethylase ALKBH3 targets single-stranded DNA (ssDNA) in order to perform DNA alkylation damage repair. ALKBH3 becomes up-regulated during tumorigenesis and is necessary for proliferation. However, the underlying molecular mechanism remains to be understood. Methods: To further elucidate the function of ALKBH3 in cancer, we performed ChIP-seq to investigate the genomic binding pattern of endogenous ALKBH3 in PC3 prostate cancer cells coupled with microarray experiments to examine the expression effects of ALKBH3 depletion. Results: We demonstrate that ALKBH3 binds to transcription associated locations, such as places of promoter-proximal paused RNA polymerase II and enhancers. Strikingly, ALKBH3 strongly binds to the transcription initiation sites of a small number of highly active gene promoters. These promoters are characterized by high levels of transcriptional regulators, including transcription factors, the Mediator complex, cohesin, histone modifiers and active histone marks. Gene expression analysis showed that ALKBH3 does not directly influence the transcription of its target genes, but its depletion induces an up-regulation of ALKBH3 non-bound inflammatory genes. Conclusions: The genomic binding pattern of ALKBH3 revealed a putative novel hyperactive promoter type. Further, we propose that ALKBH3 is an intrinsic DNA repair protein that suppresses transcription associated DNA damage at highly expressed genes and thereby plays a role to maintain genomic integrity in ALKBH3-overexpressing cancer cells. These results raise the possibility that ALKBH3 may be a potential target for inhibiting cancer progression. PC3 cells were infected with ALKBH3 shRNA or Control shRNA for 48 hours and selected with puromycine. Cells were collected after 48h or 96h past selection.
2015-06-05 | E-GEOD-57568 | biostudies-arrayexpress
Project description:Ocular melanoma is a common primary malignant ocular tumor in adults with limited effective treatments, so novel therapeutic approaches are desperately needed. Epigenetic regulation plays an important role in tumor development. The SWI/SNF chromatin remodeling complex and bromodomain and extraterminal domain (BET) family proteins are epigenetic regulators involved in several cancers. We aimed to screen a candidate small molecule inhibitor targeting the SWI/SNF complex or BET proteins and investigate its effect and mechanism in ocular melanoma. Colony formation assays were applied to select the most effective candidate inhibitor (JQ-1). We observed phenotypes caused by knockdown of the corresponding gene and synergistic effects with BRD inhibitor (BRDi) treatment and SWI/SNF complex knockdown. We further validated the efficacy of JQ-1 in 10 ocular melanoma cell lines and a mouse xenograft model. The effect of JQ-1 on ocular melanoma cell cycle and apoptosis was analyzed with flow cytometry. We performed RNA sequencing in 2 pairs of ocular melanoma cell lines treated with JQ-1 and control cells treated with DMSO. Gene set enrichment analysis (GSEA) was performed for pathway analysis of the differentially expressed genes (DEGs). We also validated the correlations of DEGs with BRD4 and patient outcomes. Overall, JQ-1 may act downstream of BRD4 and suppress ocular melanoma growth by inducing G1 cell cycle arrest.
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Project description:Background: The oxidative DNA demethylase ALKBH3 targets single-stranded DNA (ssDNA) in order to perform DNA alkylation damage repair. ALKBH3 becomes up-regulated during tumorigenesis and is necessary for proliferation. However, the underlying molecular mechanism remains to be understood. Methods: To further elucidate the function of ALKBH3 in cancer, we performed ChIP-seq to investigate the genomic binding pattern of endogenous ALKBH3 in PC3 prostate cancer cells coupled with microarray experiments to examine the expression effects of ALKBH3 depletion. Results: We demonstrate that ALKBH3 binds to transcription associated locations, such as places of promoter-proximal paused RNA polymerase II and enhancers. Strikingly, ALKBH3 strongly binds to the transcription initiation sites of a small number of highly active gene promoters. These promoters are characterized by high levels of transcriptional regulators, including transcription factors, the Mediator complex, cohesin, histone modifiers and active histone marks. Gene expression analysis showed that ALKBH3 does not directly influence the transcription of its target genes, but its depletion induces an up-regulation of ALKBH3 non-bound inflammatory genes. Conclusions: The genomic binding pattern of ALKBH3 revealed a putative novel hyperactive promoter type. Further, we propose that ALKBH3 is an intrinsic DNA repair protein that suppresses transcription associated DNA damage at highly expressed genes and thereby plays a role to maintain genomic integrity in ALKBH3-overexpressing cancer cells. These results raise the possibility that ALKBH3 may be a potential target for inhibiting cancer progression.
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Project description:In order to study the mechanism of histone lactylation, we used glycolysis inhibitors to reduce histone lactylation and applied RNA-seq and ChIP-seq to identify its target genes in ocular melanoma.
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