HCSGD entry for SPP1


1. General information

Official gene symbolSPP1
Entrez ID6696
Gene full namesecreted phosphoprotein 1
Other gene symbolsBNSP BSPI ETA-1 OPN
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

color bar
This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0001503OssificationIEAbiological_process
GO:0001649Osteoblast differentiationIEAbiological_process
GO:0005125Cytokine activityIEAmolecular_function
GO:0005576Extracellular regionTAScellular_component
GO:0005615Extracellular spaceIDAcellular_component
GO:0006954Inflammatory responseIEAbiological_process
GO:0007155Cell adhesionIEAbiological_process
GO:0007566Embryo implantationTASbiological_process
GO:0010811Positive regulation of cell-substrate adhesionIEAbiological_process
GO:0030198Extracellular matrix organizationTASbiological_process
GO:0030593Neutrophil chemotaxisIEAbiological_process
GO:0031214Biomineral tissue developmentIEAbiological_process
GO:0031988Membrane-bounded vesicleIEAcellular_component
GO:0033280Response to vitamin DIDAbiological_process
GO:0042995Cell projectionIEAcellular_component
GO:0045177Apical part of cellIEAcellular_component
GO:0045780Positive regulation of bone resorptionIEAbiological_process
GO:0046697DecidualizationTASbiological_process
GO:0048471Perinuclear region of cytoplasmIEAcellular_component
GO:0048545Response to steroid hormoneIEAbiological_process
GO:0048685Negative regulation of collateral sprouting of intact axon in response to injuryIEAbiological_process
GO:0050840Extracellular matrix bindingIEAmolecular_function
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.00073124500.88674638120.07733166021.0000000000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Up3.8478430033
GSE13712_SHEARUp0.0367781022
GSE13712_STATICDown-0.0416942273
GSE19018Down-0.0767257931
GSE19899_A1Up0.4008013908
GSE19899_A2Up1.5402373110
PubMed_21979375_A1Up1.4786557433
PubMed_21979375_A2Up2.5583756124
GSE35957Down-0.8667598306
GSE36640Down-0.0616274079
GSE54402Up1.8620234087
GSE9593Up0.8491234075
GSE43922Up2.1589563351
GSE24585Up0.0425274771
GSE37065Up0.5593706438
GSE28863_A1Down-0.2624995507
GSE28863_A2Up0.0294736344
GSE28863_A3Down-0.0287040675
GSE28863_A4Down-0.1364472272
GSE48662Up0.3273479066

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

    • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-299-5pMIMAT0002890MIRT004565immunoblot//qRT-PCR//Luciferase reporter assay//MicroarrayFunctional MTI19538464
hsa-miR-335-5pMIMAT0000765MIRT016866MicroarrayFunctional MTI (Weak)18185580
hsa-miR-146a-5pMIMAT0000449MIRT021279qRT-PCRFunctional MTI (Weak)20110513
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    • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 9 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

27165403The onset of senescence inhibited both the induction of osteoblast markers RUNX2 and osteopontin and the biomineralization of DFCs after stimulation of the osteogenic differentiation
26629698Cellular senescence is defined as an irreversible cell cycle arrest and is associated with the release of molecules known as the senescence-associated secretory phenotype that can selectively promote the growth of pre-neoplastic keratinocytes (osteopontin) and cancer invasion (transforming growth factor beta, matrix metalloproteinases, interleukin 6 and lactate)
26477312In addition to the activation of oncogenes c-MYC and STAT3 in tumor cells, a number of cytokines and growth factors, such as IL1beta, IL6 and SPP1 (osteopontin, a key biomarker for PCa), were upregulated in NFATc1-induced PCa, establishing a tumorigenic microenvironment involving both NFATc1 positive and negative cells for prostate tumorigenesis
25972477A CD153+CD4+ T follicular cell population with cell-senescence features plays a crucial role in lupus pathogenesis via osteopontin production
25972477Although the CD153(+) TF cells were defective in proliferation capacity, they were quite stable and specifically responded to self GC-B cells to secret abundant osteopontin, which inhibited B cell receptor-induced GC-B cell apoptosis in f-BWF1 mice
22340562Silencing of osteopontin promotes the radiosensitivity of breast cancer cells by reducing the expression of hypoxia inducible factor 1 and vascular endothelial growth factor
22340562BACKGROUND: Osteopontin (OPN) is a secreted phosphoglycoprotein (SSP) that is overexpressed in a variety of tumors and was regarded as a molecular marker of tumors
22340562In this study, we intended to demonstrate the role of OPN in human breast cancer cell line MDA-MB-231
22340562METHODS: Recombinant plasmid expressing small interfering RNA (siRNA) specific to OPN mRNA was transfected into MDA-MB-231 cells to generate the stable transfected cell line MDA-MB-343, and the empty plasmid tansfected cells (MDA-MB-neg) or wildtype MDA-MB-231 cells were used as control cells respectively
22340562Expression of OPN, hypoxia inducible factor-1 (HIF-1) and vascular endothelial growth factor (VEGF) proteins was analyzed by Western blotting analysis
22340562RESULTS: HIF-1 and VEGF proteins in MDA-MB-343 cells were significantly downregulated upon the efficient knockdown of OPN expression under either hypoxia or normoxia environment
22340562Moreover, expression of OPN protein was upregualted upon hypoxic culture
22340562CONCLUSIONS: Suppression of OPN gene expression can enhance radiosensitivity and affect cell apoptosis in breast cancer cells
22340562OPN seems to be an attractive target for the improvement of radiotherapy
22302986Tiam1-regulated osteopontin in senescent fibroblasts contributes to the migration and invasion of associated epithelial cells
22302986We find that stress-induced senescence induces decreased fibroblast Tiam1 protein levels and increased osteopontin levels, and that senescent fibroblast lysates induce Tiam1 protein degradation in a calcium- and calpain-dependent fashion
22302986Changes in fibroblast Tiam1 protein levels induce converse changes in osteopontin mRNA and protein
22302986These effects in epithelial cells are ameliorated by either increasing fibroblast Tiam1 or decreasing fibroblast osteopontin
22302986Finally, in seeded cell migration assays we find that either senescent or Tiam1-deficient fibroblasts induce increased epithelial cell migration that is dependent on fibroblast secretion of osteopontin
22302986These findings indicate that one mechanism by which senescent fibroblasts promote neoplastic progression in associated tumors is through degradation of fibroblast Tiam1 protein and the consequent increase in secretion of osteopontin by fibroblasts
22067611Also examined were the expression of genes involved in proliferation and mineralization such as human alkaline phosphatase (ALP), beta-actin, collagen 1 (col-1), core binding factor (cbfa-1), dentin matrix protein (DMP-1), dentin sialophosphoprotein (DSPP), GAPDH, hTERT, osteocalcin (OCN), osteopontin (OPN) as well as oncoproteins involved in senescence (p16, p21 and p53) using RT-PCR
19449178Increases in CTS-induced osteopontin (OPN) synthesis, cyclooxygenase-2 (Cox-2) mRNA expression, and nitric oxide (NO) production by osteoblasts did not change at the third and fifth passages
19155301Senescent stromal-derived osteopontin promotes preneoplastic cell growth
19155301We identified osteopontin (OPN) as one of the most highly elevated transcripts in senescent fibroblasts
19155301Importantly, reduction of OPN protein levels by RNA interference did not affect senescence induction in fibroblasts; however, it dramatically reduced the growth-promoting activities of senescent fibroblasts in vitro and in vivo, showing that OPN is necessary for paracrine stimulation of preneoplastic cell growth
19155301In addition, we found that recombinant OPN was sufficient to stimulate preneoplastic cell growth
19155301Finally, we show that OPN is expressed in senescent stroma within preneoplastic lesions that arise following 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate treatment of mice, suggesting that stromal-derived OPN-mediated signaling events affect neoplastic progression
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