Gene expression profile in prostate cancer cells after FGF13 or FGFRL1 knockdown
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA728592 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14479842.fastq.gz | Fastqsanger.gz | |||
| SRR14479843.fastq.gz | Fastqsanger.gz | |||
| SRR14479844.fastq.gz | Fastqsanger.gz | |||
| SRR14479845.fastq.gz | Fastqsanger.gz | |||
| SRR14479846.fastq.gz | Fastqsanger.gz |
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Project description:FGFRs regulate PCa development and progression, but the role of the recently found FGFR-like 1 (FGFRL1, FGFR5) remains unclear. The data consists of gene expression profiles of FGF13 and FGFRL1 knock-down PC3M prostate cancer cells compared to control cells.
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Project description:FGFRs regulate PCa development and progression, but the role of the recently found FGFR-like 1 (FGFRL1) remains unclear. The data consists of gene expression profiles of mouse subcutanous xenograft tumors generated of human PC3M prostate cancer cells with stable knockdown of FGFRL1 gene and of the control xenografts.
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Project description:Gene expression profile in prostate cancer xenograft tumors after FGFRL1 knockdown
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Project description:Purpose: This study investigates the role of fibroblast growth factor receptor-like 1 (FGFRL1) in regulating androgen receptor (AR) and fibroblast growth factor receptor (FGFR) signaling pathways in advanced prostate cancer (PCa). Methodology: Clinical samples from two independent datasets (n=48 and n=492) were analyzed to compare the expression levels of FGFRL1, AR, and FGFR1 in PCa versus normal samples. Transient knockdown (KD) experiments using siRNA were conducted in LNCaP and 22RV1 PCa cell lines to reduce FGFRL1 expression by 60-80%. FGFR downstream signaling was assessed following R1881+FGF2 stimulation. Additionally, ChIP and RNA sequencing were used to explore FGFRL1's role in AR transcriptional binding and pathway analysis. Immunohistochemistry of FGFR1 and FGFRL1 staining of tumor microarrays (n=141) were quantified for their localization pattern. Immunofluorescence and subcellular protein fractionation followed by immunoblotting were used to quantify FGFR1, FGFRL1, AR and p-AR localization in the nucleus of PCa cell lines. Results The study found elevated levels of FGFRL1 and AR, and decreased FGFR1 expression in PCa samples compared to normal prostate samples. FGFRL1 KD led to significantly reduced AR binding to androgen response elements (AREs), despite the presence of synthetic androgen R1881. This reduction in AR activity was linked to decreased expression of AR-regulated proteins, such as CAMKK2 and pAKT. FGFRL1 KD also resulted in decreased AR phosphorylation at Ser81 and reduced nuclear translocation of FGFR1. Stimulation with R1881 and FGF2 increased FGFR downstream signaling upon FGFRL1 KD, as indicated by elevated pFRS2a and pERK1/2 levels. In the PCa patient cohort (n=141), FGFR1 and FGFRL1 localization patterns were correlated, with significant positive correlations between nuclear FGFRL1 and FGFR1. Significance This study provides novel insights into the role of FGFRL1 in modulating AR and FGFR signaling in PCa. By demonstrating that FGFRL1 KD affects AR binding and FGFR1 nuclear translocation, the research highlights potential targets for developing new combinatorial therapies for advanced PCa, particularly castration-resistant prostate cancer (CRPC). Understanding the interplay between FGFR and AR signaling may offer new strategies for overcoming resistance in PCa treatment.
2026-05-20 | GSE317205 | GEO
Project description:Purpose: This study investigates the role of fibroblast growth factor receptor-like 1 (FGFRL1) in regulating androgen receptor (AR) and fibroblast growth factor receptor (FGFR) signaling pathways in advanced prostate cancer (PCa). Methodology: Clinical samples from two independent datasets (n=48 and n=492) were analyzed to compare the expression levels of FGFRL1, AR, and FGFR1 in PCa versus normal samples. Transient knockdown (KD) experiments using siRNA were conducted in LNCaP and 22RV1 PCa cell lines to reduce FGFRL1 expression by 60-80%. FGFR downstream signaling was assessed following R1881+FGF2 stimulation. Additionally, ChIP and RNA sequencing were used to explore FGFRL1's role in AR transcriptional binding and pathway analysis. Immunohistochemistry of FGFR1 and FGFRL1 staining of tumor microarrays (n=141) were quantified for their localization pattern. Immunofluorescence and subcellular protein fractionation followed by immunoblotting were used to quantify FGFR1, FGFRL1, AR and p-AR localization in the nucleus of PCa cell lines. Results: The study found elevated levels of FGFRL1 and AR, and decreased FGFR1 expression in PCa samples compared to normal prostate samples. FGFRL1 KD led to significantly reduced AR binding to androgen response elements (AREs), despite the presence of synthetic androgen R1881. This reduction in AR activity was linked to decreased expression of AR-regulated proteins, such as CAMKK2 and pAKT. FGFRL1 KD also resulted in decreased AR phosphorylation at Ser81 and reduced nuclear translocation of FGFR1. Stimulation with R1881 and FGF2 increased FGFR downstream signaling upon FGFRL1 KD, as indicated by elevated pFRS2a and pERK1/2 levels. In the PCa patient cohort (n=141), FGFR1 and FGFRL1 localization patterns were correlated, with significant positive correlations between nuclear FGFRL1 and FGFR1. Significance: This study provides novel insights into the role of FGFRL1 in modulating AR and FGFR signaling in PCa. By demonstrating that FGFRL1 KD affects AR binding and FGFR1 nuclear translocation, the research highlights potential targets for developing new combinatorial therapies for advanced PCa, particularly castration-resistant prostate cancer (CRPC). Understanding the interplay between FGFR and AR signaling may offer new strategies for overcoming resistance in PCa treatment.
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Project description:Gene expression profile of 22RV1 prostate cancer cells upon SPINK1 knockdown
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Project description:Ceramide accumulation impairs adipocytes’ ability to efficiently store and utilize nutrients, leading to energy and glucose homeostasis deterioration. Using a comparative transcriptomic screen, we identified the non-canonical, non-secreted fibroblast growth factor FGF13 as a ceramide-regulated factor that impairs adipocyte function. Obesity robustly induces FGF13 expression in adipose tissue in mice and humans and is positively associated with glycemic indices of type 2 diabetes. Pharmacological or genetic inhibition of ceramide biosynthesis reduces FGF13 expression. Using mice with loss and gain-of-function of FGF13, we demonstrate that FGF13 is both necessary and sufficient to impair energy and glucose homeostasis independent of ceramides. Mechanistically, FGF13 exerts these effects by inhibiting mitochondrial content and function, metabolic elasticity, and caveolae formation, which cumulatively impairs glucose utilization and thermogenesis. These studies suggest the therapeutic potential of targeting FGF13 to prevent and treat metabolic diseases.
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Project description:Analysis of ovarian cancer cell lines after knockdown of FGFRL1 using SiRNA. To elucidate the signaling pathways that were significantly altered following the silencing of FGFRL1 expression, we performed global gene profiling experiments of the OVCAR8 and ES2 cells after knockdown of FGFRL1 using siRNA. We conducted pathway analysis with the differentially expressed genes using R in two OC cells.
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Project description:Angiogenesis is a tightly regulated process essential for both development and disease, yet the role of fibroblast growth factor 13 (FGF13) in vascular remodeling has remained unclear. Here, we identify FGF13 as a key negative regulator of physiological and pathological angiogenesis. Using endothelial cell–specific knockout and overexpression mouse models, combined with retinal vascularization assays, hindlimb ischemia and myocardial infarction models, and in vitro endothelial cell functional assays, we demonstrate that loss of FGF13 enhances, whereas its overexpression impairs, neovascularization. Mechanistically, FGF13 binds to the PAS domain of HIF-1α and facilitates its interaction with RACK1, leading to oxygen-independent degradation of HIF-1α and suppression of downstream angiogenic signaling. Importantly, adenoviral overexpression of HIF-1α reversed the inhibitory effects of FGF13, confirming its essential role in mediating FGF13-driven angiogenic regulation. These findings reveal FGF13 as a critical endothelial-intrinsic brake on angiogenesis and suggest its potential as a therapeutic target in ischemic vascular disease.
2026-04-17 | GSE327656 | GEO
Project description:Angiogenesis is a tightly regulated process essential for both development and disease, yet the role of fibroblast growth factor 13 (FGF13) in vascular remodeling has remained unclear. Here, we identify FGF13 as a key negative regulator of physiological and pathological angiogenesis. Using endothelial cell–specific knockout and overexpression mouse models, combined with retinal vascularization assays, hindlimb ischemia and myocardial infarction models, and in vitro endothelial cell functional assays, we demonstrate that loss of FGF13 enhances, whereas its overexpression impairs, neovascularization. Mechanistically, FGF13 binds to the PAS domain of HIF-1α and facilitates its interaction with RACK1, leading to oxygen-independent degradation of HIF-1α and suppression of downstream angiogenic signaling. Importantly, adenoviral overexpression of HIF-1α reversed the inhibitory effects of FGF13, confirming its essential role in mediating FGF13-driven angiogenic regulation. These findings reveal FGF13 as a critical endothelial-intrinsic brake on angiogenesis and suggest its potential as a therapeutic target in ischemic vascular disease.
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