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Single-cell transcriptomics revealed a critical role of SPP1/CD44-mediated crosstalk between macrophages and cancer cells in glioma

ABSTRACT: Single-cell transcriptomics revealed a critical role of SPP1/CD44-mediated crosstalk between macrophages and cancer cells in glioma

PROVIDER: PRJNA768337 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16183300_1.fastq.gz	Fastqsanger.gz
	SRR16183300_2.fastq.gz	Fastqsanger.gz
	SRR16183301_1.fastq.gz	Fastqsanger.gz
	SRR16183301_2.fastq.gz	Fastqsanger.gz
	SRR16183302_1.fastq.gz	Fastqsanger.gz

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Single-cell transcriptomics revealed a critical role of SPP1/CD44-mediated crosstalk between macrophages and cancer cells in glioma

Project description:a single-cell RNA sequencing analysis of one high-grade glioma with wide-type IDH genes, revealing the landscape of tumor and immune cells in the ecosystem of this tumor

2021-10-31 | GSE185231 | GEO

Single-Cell Transcriptomic Analysis Revealed a Critical Role of SPP1/CD44-Mediated Crosstalk Between Macrophages and Cancer Cells in Glioma.

Project description: Not available

| S-EPMC8602110 | biostudies-literature

Tumor-secreted SPP1 activates CD44-Hedgehog signaling in hepatic stellate cells to promote fibrosis

Project description:Background: Advanced hepatic fibrosis is a pivotal event leading to cirrhosis and hepatocellular carcinoma (HCC). We identified osteopontin (SPP1) as a fibrosis-associated gene through transcriptome and immunohistochemical analyses and investigated its role in intratumoral fibrosis and HCC development. Methods: Gene expression analysis was conducted using publicly available datasets to screen for fibrosis-related genes. Immunohistochemical staining was performed on HCC samples to assess SPP1 expression and its correlation with fibrosis and prognosis. The biological effects of SPP1 overexpression (SPP1-OE) in HCC cells were examined in xenograft mouse models. Co-culture assay with hepatic stellate cells (HSCs) and single-cell RNA sequencing (scRNA-seq) analysis were used to explore HCC-HSC interactions. Results: Transcriptomic and prognostic analyses revealed that SPP1 was significantly upregulated in fibrotic HCC tissues and associated with unfavorable outcomes. Immunohistochemical analysis confirmed a strong correlation between SPP1 expression and intratumoral fibrosis. In xenograft models, SPP1-OE HCC cells exhibited enhanced tumor growth and extensive fibrosis. Co-culture assay demonstrated that SPP1-OE cells stimulated HSCs, and gene set enrichment analysis and differential gene expression analysis elucidated activation of the Hedgehog signaling pathway and upregulation of GLI1 in HSCs. scRNA-seq analysis discovered SPP1-CD44 signaling transduction as a key mediator of HSC activation. Pharmacological inhibition of GLI1 with the SMO inhibitor vismodegib suppressed HSC activation in vitro and reduced fibrosis and tumor growth in vivo. Conclusions: SPP1 promotes intratumoral fibrosis and HCC progression through the SPP1-CD44-GLI1 axis, highlighting its potential as a prognostic biomarker and therapeutic target. Inhibition of Hedgehog signaling may provide a promising strategy to mitigate fibrosis and improve HCC patient outcomes.

2026-03-11 | GSE290501 | GEO

SPP1 represents a therapeutic target that promotes the progression of esophageal squamous cell carcinoma by driving M2 macrophage infiltration

Project description:Background: Tumor-associated macrophages (TAMs) are an important component of the tumor microenvironment (TME). However, the crosstalk between esophageal squamous cell carcinoma (ESCC) cells and TAMs remains largely unexplored. Methods: Clinical samples and the TCGA database were used to evaluate the relevance of SPP1 and TAM infiltration in ESCC. Mouse models were constructed to investigate the roles of macrophages educated by SPP1 in ESCC. Macrophage phenotypes were determined using qRT‒PCR and immunohistochemical staining. RNA sequencing was performed to elucidate the mechanism. Results: Increasing expression of SPP1 correlated with M2-like TAM accumulation in ESCC, and they both predicted poor prognosis in the ESCC cohort. Knockdown of SPP1 significantly inhibited the infiltration of M2 TAMs in xenograft tumors. In vivo mouse model experiments showed that SPP1-mediated education of macrophages plays essential roles in the progression of ESCC. Mechanistically, SPP1 recruited macrophages and promoted M2 polarization via CD44/PI3K/AKT signaling activation and then induced VEGFA and IL6 secretion to sustain ESCC progression. Finally, blockade of SPP1 with RNA aptamer significantly inhibited tumor growth and M2 TAM infiltration in xenograft mouse models. Conclusions: This study highlights a SPP1-mediated crosstalk between ESCC cells and TAMs in ESCC. SPP1 could serve as a potential target in ESCC therapy.

2024-09-09 | GSE256360 | GEO

Xin-Zi-Sheng-Wan Decoction Alleviates Hyperuricemia-Induced Renal Injury by Modulating SPP1-CD44-Mediated Macrophage Infiltration and SRC/FAK/β-Catenin Signaling Pathway

Project description:Aim of the study This study aimed to evaluate the therapeutic efficacy of XZSWD against HUA-induced kidney injury and to elucidate the molecular pathways involved. Methods UPLC-QTOF/MS was used to identify compounds in XZSWD and medicated serum. A HUA mouse model was induced by potassium oxonate (PO) and hypoxanthine (HX) to evaluate the therapeutic effects of XZSWD on renal injury. RNA-Seq and CIBERSORT were applied to analyze gene expression and immune infiltration. Key signaling pathways were validated by qRT-PCR, Western blot, immunofluorescence, and flow cytometry. A THP-1/HK-2 co-culture system combined with SPP1 overexpression and knockdown was used to explore the molecular mechanisms underlying XZSWD’s anti-inflammatory and anti-fibrotic effects. Results 99 compounds were identified in XZSWDS. XZSWD reduced serum uric acid, improved renal function, and suppressed inflammation in HUA mice. RNA-Seq and CIBERSORT revealed downregulation of macrophage-related genes and enhanced mixed M1/M2 polarization. XZSWD inhibited the SPP1–CD44 axis and SRC/FAK/β-Catenin signaling, reducing Epithelial–Mesenchymal Transition (EMT) and Extracellular Matrix (ECM) deposition. In vitro, XZSWD suppressed uric acid-induced EMT and macrophage migration, polarization; these effects were reversed by SPP1 overexpression and enhanced by SPP1 knockdown, indicating SPP1 as a critical therapeutic target. Conclusions The XZSWD alleviates hyperuricemia-induced renal injury by effectively suppressing macrophage-mediated inflammation through coordinated regulation of the SPP1–CD44 axis and the SRC/FAK/β-Catenin signaling network.

2025-07-01 | GSE300922 | GEO

Targeting astrocytic CLC2(CLCN2) restores myelin regeneration through inhibition of SPP1/CD44 signaling pathway in leukoencephalopathy

Project description:Accumulating myelin damage and impaired remyelination are central pathological features of leukoencephalopathies, including Multiple Sclerosis and Alexander Disease, where astrocytes play essential roles in maintaining central nervous system homeostasis and mediating astrocyte-oligodendrocyte interactions. Chloride Ion Channel 2 (ClC-2), encoded by CLCN2, is functionally expressed in astrocytes and is likely critical to white matter integrity; however, its precise roles and interactions remain unclear. Clarifying the mechanisms by which astrocytic ClC-2 influences white matter is essential for developing treatments for CLCN2-related leukoencephalopathy (CC2L) and potentially other white matter disorders. In this study, we demonstrate that dysfunctional ClC-2 in astrocytes—derived from both mouse models and human-induced pluripotent stem cells (hiPSCs)—impairs oligodendrocyte lineage cell development in vitro and delays remyelination in vivo. Transcriptomic analyses identified SPP1 as a key inhibitory factor on remyelination, secreted from ClC-2-deficient astrocytes. This inhibition was validated through astrocyte-specific modulation of SPP1 expression, where overexpression exacerbated, and downregulation alleviated, demyelination effects. Furthermore, we discovered that SPP1 upregulation in astrocytes with abnormal ClC-2 negatively impacts remyelination by interacting with CD44 on oligodendrocyte progenitor cells. Finally, we confirmed that increased SPP1 expression and the resulting suppression of oligodendrocyte lineage cell development were also present in hiPSC-derived astrocytes harboring a CLCN2 mutation from a CC2L patient. Collectively, these findings reveal that astrocytic ClC-2 is intricately linked to white matter integrity through SPP1 regulation, positioning it as a potential therapeutic target for CC2L and other leukoencephalopathies.

2026-06-02 | GSE298674 | GEO

Injured tubular cells mediate neutrophil migration via Spp1/Cd44 interaction and upregulate Npm1 to promote tubular regeneration in AKI

Project description:An AKI model was induced by unilateral ischemia-reperfusion injury (uIRI) in mice, and a hypoxia/reoxygenation (H/R) model was established using TCMK-1 renal tubular epithelial cells. Transwell migration assays were conducted to validate the effect of Spp1/Cd44 interaction on peripheral blood neutrophil (PMN) migration. Proteomic analyses were used to assess protein abundance related to tubular cell regeneration. We examined the differences in protein expression in the supernatants of TCMK-1 cells co-cultured with PMNs and TCMK-1 cells cultured alone in the Transwell system.

2025-01-16 | PXD059907 |

Tumor-secreted SPP1 activates CD44-Hedgehog signaling in hepatic stellate cells to promote fibrosis

Project description:Tumor-secreted SPP1 activates CD44-Hedgehog signaling in hepatic stellate cells to promote fibrosis

| PRJNA1228515 | ENA

Targeting astrocytic CLC2(CLCN2) restores myelin regeneration through inhibition of SPP1/CD44 signaling pathway in leukoencephalopathy

Project description:Targeting astrocytic CLC2(CLCN2) restores myelin regeneration through inhibition of SPP1/CD44 signaling pathway in leukoencephalopathy

| PRJNA1270928 | ENA

Characterization of Spp1-TAP and Mer2-TAP interactomes

Project description:Histone H3K4 methylation is a feature of meiotic recombination hotspots shared by many organisms including plants and mammals. Meiotic recombination is initiated by programmed double strand break (DSB) formation that in budding yeast is directed in gene promoters by histone H3K4 di/trimethylation. This histone modification is indeed recognized by Spp1, a PHD-finger containing protein that belongs to the conserved histone H3K4 methyltransferase Set1 complex. During meiosis, Spp1 binds H3K4me and recruits a DSB protein, Mer2, to promote DSB formation close to gene promoters. How Set1C and Mer2 related functions of Spp1 are connected is not clear.

2018-01-30 | PXD007590 | Pride

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