RNA-seq of peptide RSM3 treatment in prostate cancer cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE241315 | GEO | 2024/10/09
REPOSITORIES: GEO
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Project description:Prostate cancer (PCa) is the most frequently diagnosed malignancy in men worldwide. METTL3 play nonnegligible function in PCa progression. Here, we seek to explore the effect of METTL3 on transcriptome profile in PC3 cells via RNA-seq.
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Project description:Prostate cancer (PCa) is the most frequently diagnosed malignancy in men worldwide. Epigenetic regulation has been recognized as a main mechanism of cancer evolution. PRMT5 is the major type II protein arginine methyltransferase catalyzing the symmetric dimethylation of arginine, and METTL3 is the enzymatic component of the large N6-adenosine-methyltransferase complex in mammalian responsible for N6-methyladenosine (m6A) modification in diverse RNA species. Both genes are found upregulated in PCa. However, their exact functional contribution to prostate tumorigenesis is unknown. As both proteins can regulate transcription via binding to chromatin, we seek to explore their DNA binding profiles in both AR+ LNCaP and AR- PC3 cells via recently developed CUT&Tag technique. Antibodies we used were Active Motif #61001 for PRMT5 and Abcam #195352 for METTL3. Our data suggests that both proteins regulate PCa cell biology, at least partially, through chromatin-binding and subsequent transcriptional regulation. CUT&Tag assay for arginine methyltransferase PRMT5 and N6‐adenosine‐methyltransferase METTL3 in LNCaP and PC3 cells
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Project description:PRMT5 is the major type II protein arginine methyltransferase catalyzing the symmetric dimethylation of arginine. Recent reports have indicated that PRMT5 is overexpressed in multiple cancer types, including prostate. However, the exact contribution of PRMT5 to prostate tumorigenesis is unknown. To explore the functional role of PRMT5 in prostate cancer (PCa), we knocked down PRMT5 by lentiviral shRNAs in both AR-dependent LNCaP cells and AR-independent PC3 cells. Our data suggests that PRMT5 regulates PCa cell biology. To further identify PRMT5-regulated genes in PCa, we performed paired-end RNA-seq analysis in PC3 and LNCaP cells with or without PRMT5-knockdown.
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Project description:Compared to intensely studied DNA methylation, protein methylation is less studied. PRMT5 is the major type II protein arginine methyltransferase catalyzing the symmetric dimethylation of arginine. Recent reports have indicated that PRMT5 is overexpressed in multiple cancer types, including prostate. However, the exact contribution of PRMT5 to prostate tumorigenesis is unknown. To explore PRMT5 in prostate cancer (PCa) therapeutically, we utilized a recently developed selective small molecule PRMT5 inhibitor (PRMT5i, EPZ015666) that has shown in vivo potency in MCL models. To understand the molecular mechanisms of action of PRMT5i in PCa, we performed deep RNA-seq analysis in PC3 and LNCaP cells treated with or without PRMT5i at 4 μM for 4 days in vitro.
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Project description:The function of METTL3 as an m6A writer is widely known to involve binding RNA and catalyzing m6A modification.To reveal the target gene landsCAPe of METTL3 in prostate cancer cell lines, we applied RIP-seq with a specific METTL3 antibody in PC3 and LNCAP cells.
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Project description:To explore the role of HIC1 deletion in regulating prostate cancer(PCa) microenvironment development, Human Gene Expression Microarrays were searched for altered genes upon HIC1 knockout expression in PC3 cells. According to fold-change screening between HIC1-knockout and its respective control cells, both up-regulated and down-regulated genes were shown.
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Project description:This study aimed to further our understanding of the role that hypermethylatioted in cancer 1 (HIC1) plays in prostate cancer (PCa) development. Microarrays were searched for some genes that had correlated expression with HIC1 mRNA. Our data showed that HIC1 promoter hypermethylation was presented in cell lines, tissues and plasma of PCa patients. According to fold-change screening between restoring expression of HIC1 and its respective control cells, both up-regulated and down-regulated genes were commonly observed in PC3 and C4-2B cells. The restoring expression HIC1 in PCa lines were respectively noted as PC3-HIC1 and C4-2B-HIC1 cells, and the respective controls were noted as C4-2B-GFP and PC3-GFP cells.
2012-11-17 | E-GEOD-42336 | biostudies-arrayexpress
Project description:Prostate cancer (PCa) is the most common malignant carcinoma that develops in men in Western countries. Up to 30% of patients continue to suffer from disease progression following radical prostatectomy. Therefore, better prognostic markers and molecular targets for cancer treatment are needed. MicroRNA (miRNA) has the potential to be used as biomarkers and as a therapeutic target for the treatment of various cancers, including PCa. Here, to determine how miRNA is involved in PCa progression, we investigated the miRNA expression profiles of 3 PCa cell lines, namely PC3, DU145, and LNCaP, and 2 normal prostate cell lines, namely RWPE-1 and PrSc, using miRNA microarrays. We investigated miRNA genes that were significantly upregulated in PCa cell lines (PC3, DU145, LNCaP) compared with normal cell lines (RWPE-1, PrSc).
2013-09-01 | E-GEOD-40026 | biostudies-arrayexpress
Project description:Background: Aldo-keto reductase (AKR) 1C family member 3 (AKR1C3), one of four identified human AKR enzymes, catalyzes steroid, prostaglandin, and xenobiotic metabolism. In the prostate, AKR1C3 is up-regulated in localized and advanced prostate adenocarcinoma, and is associated with prostate cancer (PCa) aggressiveness. Here we provide initial evidence for potential roles of AKR1C3 in PCa progression. Methods: Spatial distribution of AKR1C3 was analyzed using immunohistochemical staining in prostate adenocarcinoma tissue array. Human PCa PC-3 cells were stably transfected with AKR1C3 cDNA to establish PC3-AKR1C3 transfectants. Microarray and bioinformatics analyses were performed to identify pathways that are activated by elevated AKR1C3 expression in PCa cells. Functional confirmation of microarray and bioinformatics results was performed by immunoblot analysis and an in vitro Matrigel angiogenesis assay. Results: Elevated AKR1C3 expression was specifically limited to human prostate adenocarcinoma. Microarray and bioinformatics analysis suggested that elevated AKR1C3 expression in PC-3 cells modulates estradiol and androgen metabolism and activates insulin growth factor (IGF)-1 and Akt signaling pathways. Immunoblots confirmed that phosphorylated levels of IGF-1 receptor (IGF-1R) and Akt are significantly up-regulated in PC3-AKR1C3 as compared to mock transfectants. PC3-AKR1C3 transfectants promoted endothelial cell tube formation in Matrigel as compared to parental PC-3 cells and mock transfectants. Conclusion: Microarray and bioinformatics data followed by biological analyses suggest that elevated AKR1C3 expression in PC-3 cells promotes PCa angiogenesis and aggressiveness. These results suggest AKR1C3 can promote the aggressiveness of PCa through modulating estrogen and androgen metabolism with subsequent activation of growth factor IGF-1 and cytoplasmic Akt signaling pathways. Total RNA from mock- and ACR1C3 transfected PC-3 cells was isolated, with 2 or 3 biological replicates each. Gene expression data from AKR1C3 transfected PC-3 cells were compared with mock-transfected data.
2010-08-10 | E-GEOD-20956 | biostudies-arrayexpress