HCSGD entry for CXCR2

1. General information

Official gene symbolCXCR2
Entrez ID3579
Gene full namechemokine (C-X-C motif) receptor 2
Other gene symbolsCD182 CDw128b CMKAR2 IL8R2 IL8RA IL8RB
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0002407Dendritic cell chemotaxisTASbiological_process
GO:0002438Acute inflammatory response to antigenic stimulusIEAbiological_process
GO:0004871Signal transducer activityIDAmolecular_function
GO:0004918Interleukin-8 receptor activityIDAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005622IntracellularIDAcellular_component
GO:0005886Plasma membraneTAScellular_component
GO:0005887Integral component of plasma membraneTAScellular_component
GO:0006935ChemotaxisIDAbiological_process
GO:0006954Inflammatory responseTASbiological_process
GO:0006968Cellular defense responseIDAbiological_process
GO:0007165Signal transductionIDAbiological_process
GO:0007166Cell surface receptor signaling pathwayIDAbiological_process
GO:0007200Phospholipase C-activating G-protein coupled receptor signaling pathwayIDAbiological_process
GO:0007204Positive regulation of cytosolic calcium ion concentrationIEAbiological_process
GO:0008284Positive regulation of cell proliferationIDAbiological_process
GO:0009986Cell surfaceIDAcellular_component
GO:0010666Positive regulation of cardiac muscle cell apoptotic processIEAbiological_process
GO:0016020MembraneIDAcellular_component
GO:0016021Integral component of membraneIEAcellular_component
GO:0016494C-X-C chemokine receptor activityIDA IEAmolecular_function
GO:0019221Cytokine-mediated signaling pathwayIDAbiological_process
GO:0019959Interleukin-8 bindingIEA IPImolecular_function
GO:0030593Neutrophil chemotaxisIDA IEAbiological_process
GO:0030901Midbrain developmentIEAbiological_process
GO:0031623Receptor internalizationIDAbiological_process
GO:0033030Negative regulation of neutrophil apoptotic processIEAbiological_process
GO:0038112Interleukin-8-mediated signaling pathwayIDAbiological_process
GO:0042119Neutrophil activationIDAbiological_process
GO:0042629Mast cell granuleIDAcellular_component
GO:0043117Positive regulation of vascular permeabilityIEAbiological_process
GO:0045766Positive regulation of angiogenesisIEAbiological_process
GO:0070098Chemokine-mediated signaling pathwayIDAbiological_process
GO:0072173Metanephric tubule morphogenesisIEAbiological_process
GO:0090023Positive regulation of neutrophil chemotaxisIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.31608927090.91547019490.99999024731.0000000000

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

Data sourceUp or downLog fold change
GSE11954Up0.2169589028
GSE13712_SHEARDown-0.0790137558
GSE13712_STATICUp0.3080475964
GSE19018Down-0.0380234386
GSE19899_A1Up0.2739724437
GSE19899_A2Down-0.1509853190
PubMed_21979375_A1Down-0.1091884911
PubMed_21979375_A2Down-0.1236699520
GSE35957Up0.0984725400
GSE36640Up0.0519119956
GSE54402Up0.0209020587
GSE9593Up0.1910971368
GSE43922Up0.0174332408
GSE24585Up0.2931481160
GSE37065Up0.0248970199
GSE28863_A1Up0.0177980800
GSE28863_A2Up0.0250863719
GSE28863_A3Up0.1922068106
GSE28863_A4Down-0.0000874598
GSE48662Up0.0707889932

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-335-5pMIMAT0000765MIRT017358MicroarrayFunctional MTI (Weak)18185580
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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: 5 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

23869868Chemokine receptor CXCR2 is transactivated by p53 and induces p38-mediated cellular senescence in response to DNA damage
23869868Chemokine receptor CXCR2 was previously reported to mediate replicative and oncogene-induced senescence in a DDR and p53-dependent manner
23869868Here, we report that CXCR2 is upregulated in various types of cells in response to genotoxic or oxidative stress
23869868Unexpectedly, we found that the upregulation of CXCR2 depends on the function of p53
23869868Like other p53 target genes such as p21, CXCR2 is transactivated by p53
23869868We identified a p53-binding site in the CXCR2 promoter that responds to changes in p53 functional status
23869868Thus, CXCR2 may act downstream of p53
23869868While the senescence-associated secretory phenotype (SASP) exhibits a kinetics that is distinct from that of CXCR2 expression and does not require p53, it reinforces senescence
23869868Our results thus demonstrate CXCR2 as a critical mediator of cellular senescence downstream of p53 in response to DNA damage
23597430IL-8 also increased telomerase activity which was accompanied with upregulation of the catalytic subunit, telomerase reverse transcriptase (TERT), whereas these effects were significantly attenuated by SB 225002 (selective non-peptide CXCR2 antagonist)
22789011Human pituitary tumor-transforming gene 1 overexpression reinforces oncogene-induced senescence through CXCR2/p21 signaling in breast cancer cells
22789011The interplay between hPTTG1 overexpression and chemokine C-X-C motif receptor 2 (CXCR2)/p21-dependent senescence in tumor growth and metastasis of MCF-7 cells was investigated by orthotopic transplantation of severe combined immunodeficiency (SCID) mice
22789011Additionally, human invasive ductal carcinoma (IDC) tissue arrays were used to confirm the hPTTG1/CXCR2/p21 axis established in vitro
22789011Herein, we showed that hPTTG1 overexpression reinforced senescence through the CXCR2/p21 signaling
22789011Furthermore, hPTTG1 overexpression activated NF-kappaB signaling to transactivate the expression of interleukin (IL)-8 and growth-regulated oncogene alpha (GROalpha) to execute CXCR2 signaling in MCF-7 cells
22789011When CXCR2 expression was knocked down in hPTTG1-overexpressing MCF-7 cells, hPTTG1-induced senescence was abrogated by alleviating CXCR2-induced p21 expression
22789011Moreover, CXCR2 knockdown in hPTTG1-overexpressing MCF-7 tumors dramatically accelerated tumor growth and metastasis
22789011Our in vitro and in vivo results demonstrated that hPTTG1 overexpression reinforces senescence through CXCR2 signaling, and the evasion of CXCR2/p21-dependent senescence was critical to hPTTG1 exerting its oncogenic potential
22789011Immunohistochemical analysis of human breast tumor samples also confirmed the importance of the hPTTG1/CXCR2 axis in promoting breast cancer metastasis
18838863Control of senescence by CXCR2 and its ligands
18555777Chemokine signaling via the CXCR2 receptor reinforces senescence
18555777Here, we report that knocking down the chemokine receptor CXCR2 (IL8RB) alleviates both replicative and oncogene-induced senescence (OIS) and diminishes the DNA-damage response
18555777Conversely, ectopic expression of CXCR2 results in premature senescence via a p53-dependent mechanism
18555777Cells undergoing OIS secrete multiple CXCR2-binding chemokines in a program that is regulated by the NF-kappaB and C/EBPbeta transcription factors and coordinately induce CXCR2 expression
18555777CXCR2 upregulation is also observed in preneoplastic lesions in vivo
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