Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA246718 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcription profiling by high throughput sequencing of c-JUN and JUND knockdown prostate cancer PC3 cell lines
2025-01-24 | E-GEOD-53470 | ExpressionAtlas
Project description:Genome-wide expression profiling of SGTA knockdown in C4-2B prostate cancer cells
2025-01-24 | E-GEOD-43521 | ExpressionAtlas
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: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.
2015-06-05 | GSE57591 | GEO
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.
2015-06-05 | GSE57568 | GEO
Project description:MELK and UBE2C gene knockdown in prostate cancer cell line PC3
| PRJNA146599 | ENA
Project description:Genes regulated by GRK3 in PC3 prostate cancer cells
| PRJNA151745 | ENA
Project description:Tumor-derived extracellular vesicles (EVs) play an important role in cancer pro-gression. Neutral Sphingomyelinases (nSMases) are lipid modifying enzymes that modu-late the secretion of EVs from cells. How nSMase activity and therefore ceramide genera-tion affects the composition and functionality of secreted EV is not fully understood. Here, we aimed to investigated the expression of nSMases 1 and 2 in prostate cancer (PCa) tissue and their role in EV composition and secretion for prostate cancer cell migration. Reduced nSMase 1 and 2 expression was found in prostate cancer and correlated with age of pa-tients. When nSMase 2 was inhibited by GW4869 in PCa cells, PC3 and DU145, the EV se-cretome was significantly altered, while the number of EVs and total protein content of the released EVs were not significantly changed. Using proteomics analysis, we found extra-cellular matrix proteins, such as SDC4 (Syndecan-4) and SRPX-2 differentially secreted on EVs from GW4869-treated PC3 cells. In scratch wound migration assays, GW4869 signifi-cantly increased migration compared to control PC3 cells but not DU145 cells, while SDC4 knockdown significantly reduced migration of PC3 cells. These and other nSMase 2-dependent secreted proteins are interesting candidates to understand the role of stress-induced EV in the progression of prostate cancer.
2025-05-07 | PXD062469 | Pride
Project description:Microarray analysis of PC3 prostate tumor-initiating cells (PC3 holoclones)
| PRJNA227068 | ENA
Project description:In order to address the putative role of MELK and UBE2C in prostate cancer development and progression, we performed functional analysis upon siRNA-based knockdown, and searched for downstream genes and processes by microarray experiments. RNAi-based inhibition of MELK and UBE2C was efficient in PC3 prostate cancer cells and decreased transcriptional level down to about 30% remaining expression level. Illumina microarray experiments were done upon siRNA based knockdown 48h after transfection of PC3 cells in triplicates.
2012-10-19 | E-GEOD-32873 | biostudies-arrayexpress