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Upregulation of GALNT7 in prostate cancer modifies O-glycosylation and promotes tumour growth

ABSTRACT: To identify signalling pathways altered by GALNT7 in prostate cancer cells, we established DU145 and CWR22Rv1 stable cell lines in which GALNT7 was overexpressed or knocked down, respectively. We then performed differential gene expression and Gene Ontology analyses using data obtained from RNA-seq of the control and OE/KD cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE220942 | GEO | 2023/02/14

REPOSITORIES: GEO

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Upregulation of GALNT7 in prostate cancer modifies O-glycosylation and promotes tumour growth.

Project description:Prostate cancer is the most common cancer in men and it is estimated that over 350,000 men worldwide die of prostate cancer every year. There remains an unmet clinical need to improve how clinically significant prostate cancer is diagnosed and develop new treatments for advanced disease. Aberrant glycosylation is a hallmark of cancer implicated in tumour growth, metastasis, and immune evasion. One of the key drivers of aberrant glycosylation is the dysregulated expression of glycosylation enzymes within the cancer cell. Here, we demonstrate using multiple independent clinical cohorts that the glycosyltransferase enzyme GALNT7 is upregulated in prostate cancer tissue. We show GALNT7 can identify men with prostate cancer, using urine and blood samples, with improved diagnostic accuracy than serum PSA alone. We also show that GALNT7 levels remain high in progression to castrate-resistant disease, and using in vitro and in vivo models, reveal that GALNT7 promotes prostate tumour growth. Mechanistically, GALNT7 can modify O-glycosylation in prostate cancer cells and correlates with cell cycle and immune signalling pathways. Our study provides a new biomarker to aid the diagnosis of clinically significant disease and cements GALNT7-mediated O-glycosylation as an important driver of prostate cancer progression.

| S-EPMC10020086 | biostudies-literature

Sialic acid blockade inhibits the metastatic spread of prostate cancer to bone

Project description:To identify signalling pathways altered by GSM6829 in prostate cancer cells, we established DU145 stable cell lines in which ST6GAL1 was overexpressed. We then performed differential gene expression, Gene Ontology and GSEA analyses using data obtained from RNA-seq of the control and OE cell lines.

2024-12-31 | GSE236208 | GEO

Upregulation of GALNT7 in prostate cancer modifies O-glycosylation and promotes tumour growth

Project description:Upregulation of GALNT7 in prostate cancer modifies O-glycosylation and promotes tumour growth

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The role of GCNT1 mediated O-glycosylation in aggressive prostate cancer.

Project description:To identify signalling pathways altered by GCNT1 in prostate cancer cells, we established PC3 stable cell lines in which GCNT1 was overexpressed. We then performed differential gene expression, Gene Ontology and GSEA analyses using data obtained from RNA-seq of the control and OE cell lines.

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Effect of depletion of RAD51 on gene expression in Huh7 cells

Project description:To investigate the role of RAD51 in HCC, we established Huh7 cell lines in which RAD51 has been knocked down(KD) by sgRNA,we performed RNA-seq for RAD51-KD Huh7 cells and parental Huh7 cells(control group,sgcon).

2023-05-17 | GSE216728 | GEO

DNA-PKcs is a key transcriptional and splicing regulator of AR-Vs in advanced prostate cancer

Project description:To investigate the role of DNA-PKcs and RBMX in the regulation of androgen receptor variants we used the CWR22Rv1-AR-EK and CWR22Rv1 cell line in which DNA-PKcs or RBMX has been knocked down by siRNA or DNA-PKcs was inhibited with 1 µM NU7441, NU5455 or AZD7648. We then performed gene expression analysis using data obtained from RNA-seq at two time points (72 hours knockdown and 24 hours drug treatment).

2023-09-11 | GSE242255 | GEO

Cilia and the exocyst are involved in urinary extracellular vesicle production and content

Project description:A recently proposed model of cell-cell communication, called “urocrine signaling”, hypothesizes that small (50-150 mm) extracellular vesicles (EVs) carry signals to “downstream” kidney tubule cells. We previously showed that the exocyst, a highly-conserved eight-protein (Exoc1-8) trafficking complex, is necessary for ciliogenesis, we show that the EV number released from MDCK cells was increased in EXOC5 OE, while it was decreased in Exoc5 KD, compared to control. To determine how Exoc5 changes the composition of EVs, we isolated EVs from Exoc5 control, KD, and OE MDCK cells, and subjected them mass spectrometry-based proteomic analysis to determine the protein composition of the EVs. By dendrogram, heat map, and principle component analysis, the protein content of the EVs was significantly different in Exoc5 KD, EXOC5 OE, and control MDCK cells. To confirm the proteomic results, we examined, by Western blot analysis, expression of the small guanosine triphosphate (GTP)-binding protein ADP-ribosylation factor (Arf6) and the epidermal growth factor receptor kinase substrate 8-like protein 2 (Eps8L2).

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EphA6 promotes angiogenesis and prostate cancer metastasis and is associated with human prostate cancer progression

Project description:Purpose: Metastasis remains the primary cause of prostate cancer (CaP) related death. Here, we investigate the molecular, pathologic, and clinical outcome associations of EphA6 expression and its role in CaP progression and metastasis.Experimental Design: The gene expression profiling of Eph receptors (Ephs) and their ephrin ligands was performed in CaP cell lines by real-time RT-PCR. Metastatic potential of EphA6 gene was analyzed by RNAi approaches in a spontaneous CaP mouse model. The mRNA expression of EphA6 was measured in 58 benign prostate hyperplasia (BPH) and 112 CaP samples. Results: Among the tested Ephs and ligands, EphA6 is the only consistently overexpressed member in CaP lymph node metastatic cells. EphA6 knock-down (KD) in human PC-3M cells causes decreased invasion in vitro and reduced lung and lymph node metastasis in vivo. In addition, KD of EphA6 decreases tube formation in vitro and angiogenesis in vivo. Studies on the clinical samples demonstrate that EphA6 is overexpressed in the CaP tumor tissues compared with those from BPH patients. The correlation was identified between EphA6 expression and vascular invasion (P=0.004), neural invasion (P=0.002), PSA level (P=0.013), and TNM staging (P=0.021) in 112 CaP cases.Further, genome-wide gene expression analysis in KD of EphA6 cells identified a panel of genes, such as PIK3IPA, AKT1, and EIF5A2, which could be associated with EphA6-regulated cancer progression. Conclusions: These findings identify EphA6 as a potentially novel metastasis gene, and increased EphA6 mRNA expression positively correlates with CaP progression. The mechanisms to inhibit EphA6 expression might suppress CaP metastatic aggressiveness. Knock-down of EphA6 induced gene expression in human prostate cell:PC-3M/shEphA6-1, PC3M/shControl, CWR22rv1/shEphA6-1, and CWR22rv1/shControl cell line.

2015-02-27 | E-GEOD-66335 | biostudies-arrayexpress

Transcriptome profiling of OsbZIP48 rice transgenics

Project description:Rice transgenic plants of the bZIP encoding gene, OsbZIP48, in the Pusa Basmati 1 (PB1) variety have been found to display differences in the total height. In order to elucidate changes at the transcriptome level, microarray of the 10-day-old seedlings of over-expresseion (OE) and knock-down (KD) lines along with vector control (VC) were carried out.

2017-10-11 | GSE90472 | GEO

Small RNA-seq datasets of OsRDR4 transgenic plants

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2022-01-31 | GSE181778 | GEO

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