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SFRP2 Overexpression Induces an Osteoblast-Like Phenotype in Prostate Cancer Cells

ABSTRACT: SFRP2 Overexpression Induces an Osteoblast-Like Phenotype in Prostate Cancer Cells

PROVIDER: PRJNA901505 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22287485_1.fastq.gz	Fastqsanger.gz
	SRR22287485_2.fastq.gz	Fastqsanger.gz
	SRR22287486_1.fastq.gz	Fastqsanger.gz
	SRR22287486_2.fastq.gz	Fastqsanger.gz
	SRR22287487_1.fastq.gz	Fastqsanger.gz

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SFRP2 Overexpression Induces an Osteoblast-Like Phenotype in Prostate Cancer Cells

Project description:Abstract: Prostate cancer bone metastasis is still one of the most fatal cancer diagnosis for men. Survival of the circulating prostate tumor cells and their adaptation strategy to survive in the bone niche is the key point to determining metastasis in early cancer stages. The promoter of SFRP2, a WNT signaling regulator, is hypermethylated in many cancer types including prostate cancer. Moreover, SFRP2 can positively modulate osteogenic differentiation in vitro and in vivo. Here, we showed SFRP2 overexpression in the prostate cancer cell line PC3 induces an epithelial mesenchymal transition (EMT), increases the attachment, and modifies the transcriptome towards an osteoblast-like phenotype (osteomimicry) in a collagen 1‑dependent manner. Our data reflects a novel molecular mechanism how metastasizing prostate cancer cells might increase their chance to survive within bone tissue.

2022-12-16 | GSE217979 | GEO

RNA-seq of human glioblastoma cell lines with overexpression of SOX2, SFRP2

Project description:Glioblastomas type A cell line (U-2987) was transfected with pLEX-blast-V5-YFP (control), and pLEX-blast-V5-SFRP2 (SFRP2), and type B cell culture (U-2982, U-343 MG) were transfected with pLEX-blast-V5-YFP (control), and pLEX-blast-V5-SOX2 (SOX2). Then RNA-seq was performed and used to analyse their regulation in the gene expression level.

2021-06-01 | E-MTAB-7591 | biostudies-arrayexpress

SFRP2 modulates functional phenotype transition and energy metabolism of macrophages during diabetic wound healing [Skin wound]

Project description:Diabetic foot ulcer (DFU) is a serious complication of diabetes mellitus, which causes great health damage and economic burden to patients. The pathogenesis of DFU is not fully understood.We screened wound healing-related genes using bioinformatics analysis, and full-thickness skin injury mice model and cellular assays were used to explore the role of target genes in diabetic wound healing. SFRP2 was identified as a wound healing-related gene, and the expression of SFRP2 is associated with immune cell infiltration in DFU. In vivo study showed that suppression of SFRP2 delayed the wound healing process of diabetic mice, impeded angiogenesis and matrix remodeling, and increased macrophage infiltration in wound tissues. In addition, suppression of SFRP2 enhanced M1 polarization in both the early and later stage of wound healing, and decreased M2 polarization in the later stage, which impeded the transition of M1 to M2 polarization of wound healing. Moreover, suppression of SFRP2 affected the transcriptome signatures-related to inflammatory response and energy metabolism at the early stage of wound healing. Extracellular flux analysis (EFA) showed that suppression of SFRP2 decreased mitochondrial energy metabolism and increased glycolysis in injury-related macrophages. Furthermore, suppression of SFRP2 inhibited transcriptome signaturesrelated to carbohydrate metabolism, lipid metabolism and amino acid metabolism, which consists the three main components of energy metabolism of macrophages. In conclusions, SFRP2 may function as a wound healing-related gene in DFU, and suppression of SFRP2 impaired diabetic wound healing by compromising the M1-to-M2 transition of macrophages and modulating the balance between mitochondrial energy metabolism and glycolysis.

2024-10-04 | GSE268760 | GEO

SFRP2 modulates functional phenotype transition and energy metabolism of macrophages during diabetic wound healing [RAW264.7 cells]

2024-10-04 | GSE268759 | GEO

Gene expression changes induced by SFRP2 silencing in RB383 retinoblastoma cells

Project description:To gain insight into signaling downstream of SFRP2 in retinoblastoma, we used siRNA to silence SFRP2 in RB383 retinoblastoma cells and assessed the resulting gene expression changes at 24 hours and 48 hours after siRNA transfection.

2023-08-21 | GSE161990 | GEO

SFRP2+ CAFs Hinder Abscopal Effect from Combined Radiotherapy and Immunotherapy by Forming a Hostile Perivascular Niche

Project description:Despite accumulating cases of radiotherapy-induced abscopal effect in the lung cancer with the introduction of immune checkpoint inhibitors (ICIs), the occurrence of this effect remains infrequent and unpredictable to be a therapeutic goal. Here, we showed that the combination of radiotherapy (8Gy*3F) and ICI alleviated the tumor burden at the irradiated site whereas no discernible benefit was observed in the abscopal tumors. RNA-sequencing data showed that extracellular structure organization pathways were enriched in the abscopal tumors after combined therapy, with Sfrp2 being identified as a central hub. SFRP2 expression was observed in cancer-associated fibroblasts (CAFs) and was elevated in abscopal tumors after combined therapy. Blockade of SFRP2 followed by combined radiotherapy and ICI reinvigorated infiltration and cytotoxicity of CD8+ T cells, and elicited regression of abscopal tumors, which was abrogated by CD8α depletion. Mechanistically, in vitro experiments demonstrated that SFRP2+ CAFs induced apoptosis of CD8+ T cells. The spatial transcriptome analysis showed that SFRP2+ CAFs were located in proximity to the vessels and surrounded by abundant macrophages and limited CD8Tex, thereby creating an immunosuppressive perivascular niche, which was validated in paraffin sections of human lung cancer. Lineage-tracing assays showed SFRP2+ CAFs were derived from pericytes. IGF-1 released by irradiated tumors facilitated the transition of pericytes into fibroblasts and stimulated the expression of SFRP2. In summary, SFRP2+ CAFs hijack the abscopal effect from combined radiotherapy and immunotherapy via inducing apoptosis of CD8+ T cells and orchestrating a hostile perivascular niche in the lung cancer. Targeting SFRP2+ CAF may recondition the TME and promote the abscopal effect.

2024-04-01 | GSE261799 | GEO

Cyproconazole induces altered expression of adipogenic and osteoblast genes in zebrafish

Project description:Cyproconazole induces altered expression of adipogenic and osteoblast genes in zebrafish

| PRJNA899474 | ENA

SFRP2 modulates functional phenotype transition and energy metabolism of macrophages during diabetic wound healing [Skin wound]

Project description:SFRP2 modulates functional phenotype transition and energy metabolism of macrophages during diabetic wound healing [Skin wound]

| PRJNA1118699 | ENA

SFRP2 modulates functional phenotype transition and energy metabolism of macrophages during diabetic wound healing [RAW264.7 cells]

Project description:SFRP2 modulates functional phenotype transition and energy metabolism of macrophages during diabetic wound healing [RAW264.7 cells]

| PRJNA1118696 | ENA

FGF19 induces the inflammatory phenotype of LX-2 cells

Project description:FGF19 induces the inflammatory phenotype of LX-2 cells

| PRJNA891228 | ENA