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GENE:
SPP1 (Secreted Phosphoprotein 1)
i
Other names: SPP1, Secreted Phosphoprotein 1, Osteopontin, Early T-Lymphocyte Activation 1, Urinary Stone Protein, Nephropontin, Uropontin, BNSP, OPN, Secreted Phosphoprotein 1 (Osteopontin, Bone Sialoprotein I, Early T-Lymphocyte Activation 1), Osteopontin/Immunoglobulin Alpha 1 Heavy Chain Constant Region Fusion Protein, Secreted Phosphoprotein 1 Variant 6, SPP1/CALPHA1 Fusion, Bone Sialoprotein 1, Bone Sialoprotein I, ETA-1, SPP-1, BSPI
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Owing to the fact that the Editorial Office has been made aware of the possibility of inappropriate statistics handling in this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Molecular Medicine Reports 1: 641‑646, 2008; DOI: 10.3892/mmr_00000005].
Ectopic expressions of DNMT1 impose an epigenetic checkpoint at those target loci by methylation of promoter DNA of the respective genes. We conclude that, gene specific hypomethylation of some genes, including COL1A1, COL1A2, COL4A1, SPP1, SPARC, and THBS2 drives COAD and would serve as potential markers for COAD screening.
3 days ago
Journal
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EGFR (Epidermal growth factor receptor) • SPP1 (Secreted Phosphoprotein 1) • DNMT1 (DNA methyltransferase 1) • COL1A1 (Collagen Type I Alpha 1 Chain) • THBS2 (Thrombospondin 2) • COL4A1 (Collagen Type IV Alpha 1 Chain)
Our study demonstrates that the OPN/PI3K/AKT/CSF1-CSF1R axis plays a crucial role in CRC metastasis. Blocking the CSF1/CSF1R axis reduces M2-like TAMs infiltration and tumor metastasis, offering a promising strategy for metastatic CRC.
This review summarizes the mechanisms by which TAMs and CAFs contribute to resistance to ICIs and TKIs and discusses therapeutic strategies under active investigation targeting these stromal components-including inhibition of TGF-β, IL-6, and HGF/MET pathways, TAM reprogramming via PI3Kγ or CD47 blockade, and CAF depletion using FAP-targeted approaches. Targeting the TME holds promise for overcoming therapeutic resistance and improving clinical outcomes in advanced HCC, warranting further evaluation in well-designed clinical trials.
This study establishes a pan-skin cancer immune remodelling framework, providing a foundation for biomarker discovery and the development of new immunotherapy strategies.
Our comprehensive analysis of cell-cell communication networks among epithelial cells, fibroblasts, macrophages, and lymphocytes across BC subtypes focuses on ligand-receptor interactions. This study revealed that certain molecules within these networks exhibit significant prognostic value and therapeutic promise.
In a macrophage-depleted murine CRC model established with clodronate (CL2MDP) liposomes and MC38 cells, macrophage depletion significantly inhibited tumor growth, accompanied by reduced SPP1 expression and increased infiltration of CD8⁺ T cells and type 1 cytotoxic T (Tc1) cells...These effects were attenuated by SPP1 neutralization or CD44 inhibition. Collectively, these findings elucidated TAM-derived SPP1 as a key mediator of immune suppression in CRC and suggested that the TAM-SPP1 axis is a potential therapeutic target.
miR-4458 is highly expressed in AS, which can promote the transformation of smooth muscle cells (SMCs) to smooth muscle cells (SEMs), as well as the proliferation and migration of SMCs, thereby accelerating the progression of AS. Interaction between the miR-4458/PRTG axis and retinoic acid (RA) signaling pathway could be harnessed therapeutically to modulate VSMC phenotype in ox-LDL-induced AS.
The inhibition of OPN increased GBM sensitivity to temozolomide (TMZ) in orthotopic models. This study revealed the potential mechanism by which hypoxia-induced OPN+ GAMs promote the mesenchymal transition in GBM cells and demonstrated the therapeutic potential of targeting OPN to enhance TMZ treatment effectiveness.
Diff-Metabolic cells retained liver-specific functions with favorable prognosis, whereas the other three programs correlated with disease advancement; notably, all four states exhibited differential therapeutic vulnerabilities, including sorafenib resistance...Geneformer-based virtual knockout screening identified HSP90B1 as a convergent dependency, validated by its cancer cell essentiality, HCC overexpression, abundance in treatment-resistant tumors, and association with adverse survival. This integrated atlas establishes a framework for targeting tumor-intrinsic states and microenvironmental dependencies in HCC.
8 days ago
Journal
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SPP1 (Secreted Phosphoprotein 1) • CD36 (thrombospondin receptor) • TGFB1 (Transforming Growth Factor Beta 1) • HSP90AB1 (Heat Shock Protein 90 Alpha Family Class B Member 1) • POSTN (Periostin) • ESM1 (Endothelial Cell Specific Molecule 1)
This study delineates the mechanism that TREM2+ TAMs promote LN metastasis in HNSCC by facilitating CD8+ T cells exhaustion via SPP1-CD44-BHLHE40 axis, proposing TREM2+ TAMs as potential therapeutic target for HNSCC.