INT127691

Context Info Confidence 0.66 First Reported 2005 Last Reported 2011 Negated 0 Speculated 0 Reported most in Body Documents 23 Total Number 25 Disease Relevance 18.11 Pain Relevance 7.04

cell proliferation (CXCL1) signal transduction (CXCL1) extracellular space (CXCL1) extracellular region (CXCL1) intracellular (CXCL1)

Anatomy Link Frequency pancreas 2 T cell 2 neutrophil 2 plasma 1 brain 1 CXCL1 (Homo sapiens)

Pain Link Frequency Relevance Heat Inflammation 438 100.00 chemokine 289 100.00 cytokine 67 100.00 addiction 3 100.00 ischemia 102 99.56 cINOD 9 98.52 dexamethasone 6 97.44 corticosteroid 27 96.88 anesthesia 20 93.20 rheumatoid arthritis 154 92.08

Disease Link Frequency Relevance Heat INFLAMMATION 461 100.00 Adhesions 102 100.00 Obesity 18 99.84 Metastasis 23 99.72 Cv Unclassified Under Development 48 99.56 Colon Cancer 72 99.44 Polyps 87 98.84 Adenoma 109 98.76 Increased Venous Pressure Under Development 114 98.72 Pancreatitis 3 98.56

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CXCL1 expression is up-regulated in colorectal adenomas and adenocarcinoma [17], inhibiting apoptosis and inversely linked to expression of fibulin-1, an extra-cellular matrix protein implicated in control of tumour cell migration.

Gene_expression (expression) of CXCL1 associated with adenocarcinoma, adenoma, cancer and apoptosis

1) Confidence 0.66 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3017541 Disease Relevance 1.74 Pain Relevance 0.25

Wang et al. (2006) [18] reported that expression of CXCL1 induced by PGE2 was linked to angiogenesis in colorectal cancer in vitro and in vivo and thus provided a link between COX-2 up-regulation and chemokine induced tumour associated endothelial cell migration.

Gene_expression (expression) of CXCL1 in endothelial cell associated with colorectal cancer, chemokine and cancer

2) Confidence 0.66 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3017541 Disease Relevance 1.60 Pain Relevance 0.22

Candesartan reduced CXCL1 gene expression within the border of the ischemic lesion.

Gene_expression (expression) of CXCL1 gene

3) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2993950 Disease Relevance 1.07 Pain Relevance 0.25

Gene expression of CXCL1, interleukin-6 and TNF-alpha was upregulated in ischemic brain areas of dTGR (Fig. 5).

Gene_expression (expression) of CXCL1 in brain

4) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2993950 Disease Relevance 0.37 Pain Relevance 0.04

Only aliskiren was able to reduce gene expression of CXCL1, interleukin-6 and TNF-alpha in the ischemic core.

Gene_expression (expression) of CXCL1

5) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2993950 Disease Relevance 1.00 Pain Relevance 0.22

Pre-treatment with candesartan or aliskiren attenuated this increase of CXCL1 expression 24 h post-ischemia.

Gene_expression (expression) of CXCL1 associated with ischemia

6) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2993950 Disease Relevance 1.16 Pain Relevance 0.44

Pretreatment with BQ-123 or BQ-788 (i.a.; 15 pmol/cavity) also decreased zymosan-induced TNF-alpha production within 6 h, keratinocyte-derived chemokine/CXCL1 production within 24 h, and leukotriene B(4) at both time-points.

Gene_expression (production) of CXCL1 in keratinocyte associated with chemokine

7) Confidence 0.58 Published 2008 Journal J. Leukoc. Biol. Section Abstract Doc Link 18515326 Disease Relevance 1.09 Pain Relevance 0.52

In addition, IL-8, CXCL1, CXCL2, CXCL3, and CCL20 had higher levels of expression in the polyps compared to normal, which is in keeping with the current study.

Gene_expression (had) of CXCL1 associated with polyps

8) Confidence 0.57 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3017541 Disease Relevance 1.30 Pain Relevance 0.26

Relative gene expression of CXCL1, interleukin-6 and TNF-alpha was significantly reduced in the ischemic core of dTGR treated with aliskiren (p<0.05).

Gene_expression (expression) of CXCL1

9) Confidence 0.49 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2993950 Disease Relevance 0.37 Pain Relevance 0.04

In contrast, in the ischemic border zone there was a significant reduction of CXCL1 gene expression in animals treated with candesartan (p<0.01).

Gene_expression (expression) of CXCL1 gene

10) Confidence 0.49 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2993950 Disease Relevance 0.44 Pain Relevance 0.03

Arterial SMCs, in particular, express a large set of genes that mediate these interactions—such as cytokines/chemokines (IL6, CCL8, CCL7, CCL2, CXCL1, CXCL2, CXCL3, and CXCL6), complement pathway (complement factor B [CFB]), and surface receptor (ICAM1) (Figure 3B)—suggesting that vascular SMCs may themselves mediate recruitment of immune cells to the vascular walls.

Gene_expression (express) of CXCL1 in immune cells associated with chemokine and cytokine

11) Confidence 0.43 Published 2007 Journal PLoS Genetics Section Body Doc Link PMC1994710 Disease Relevance 0.17 Pain Relevance 0.10

Among CXC chemokines, IL-8/CXCL8, epithelial neutrophil-activating protein-78 (ENA-78)/CXCL5, growth-regulated oncogene-alpha (gro?)

Gene_expression (gro) of growth-regulated oncogene-alpha in neutrophil associated with chemokine

12) Confidence 0.32 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2592799 Disease Relevance 0.44 Pain Relevance 0.61

Among CXC chemokines, IL-8/CXCL8, epithelial neutrophil-activating protein-78 (ENA-78)/CXCL5, growth-regulated oncogene-alpha (gro?)

Gene_expression (/) of growth-regulated oncogene-alpha in neutrophil associated with chemokine

13) Confidence 0.32 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2592799 Disease Relevance 0.50 Pain Relevance 0.63

/CXCL1, connective tissue-activating peptide-III (CTAP-III)/CXCL7, granulocyte chemotactic protein-2/CXCL6, IP-10/CXCL10, PF4/CXCL4, monokine induced by IFN-?

Gene_expression (connective tissue) of CXCL1 in granulocyte

14) Confidence 0.32 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2592799 Disease Relevance 0.43 Pain Relevance 0.61

This conclusion is supported, at least in part, by the results of Sukumaran and colleagues [52], who reported the upregulated expression of chemokine genes encoding CXCL1, CXCL2, CXCL3, CXCL8, CCL3, CCL4 and CCL20 after infection of PMN with Anaplasma phagocytophilum.

Gene_expression (expression) of CXCL1 associated with chemokine and infection

15) Confidence 0.24 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.58 Pain Relevance 0.50

The disparity in angiogenic activity among CXC chemokine family members is attributed to three amino acid structural domains at the N terminus, Glu-Leu-Arg (ELR), which is present in angiogenic (i.e., CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL7, and CXCL8) [4-6], but not angiostatic (i.e., CXCL4, CXCL9, CXCL10, and CXCL11) CXC chemokines [7].

Gene_expression (present) of CXCL1 associated with chemokine

16) Confidence 0.23 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2895614 Disease Relevance 0.64 Pain Relevance 0.27

CXCL6 also has angiogenesis activity and can stimulate cancer cell progression.26,27 Zhu et al reported overexpression of CXCL6 with its receptor, IL8R, in hypoxic small cell lung cancer, which is an autocrine regulation for cell progression.28 Rubie et al observed an overexpression of CXCL1 and CXCL5 in CRC, but the level of CXCL6 was not changed.29 Our observations showed that copy number loss and low expression levels were correlated with the invasiveness of CRC.

Gene_expression (overexpression) of CXCL1 in lung associated with lung cancer, hypoxia, cancer and colon cancer

17) Confidence 0.20 Published 2010 Journal Cancer Informatics Section Body Doc Link PMC2918356 Disease Relevance 0.68 Pain Relevance 0.16

Increases in gene expression of IL-8, GRO-alpha, MCP-1, and RANTES in response to TNF-alpha treatment were detected.

Gene_expression (expression) of GRO-alpha

18) Confidence 0.16 Published 2005 Journal J. Oral Pathol. Med. Section Body Doc Link 15946184 Disease Relevance 0.14 Pain Relevance 0

As observed above, ICAM-1, IL-6, IL-8, GM-CSF, RANTES, MCP-1, GROalpha, NAP-2, and ENA-78 expression was reduced by the IKK inhibitors.

Gene_expression (expression) of GROalpha

19) Confidence 0.13 Published 2006 Journal Mol. Pharmacol. Section Abstract Doc Link 16687566 Disease Relevance 0.42 Pain Relevance 0.41

IL33 rapidly induced the phosphorylation of MAPKs and IkappaBalpha, and enhanced the expression of inflammatory mediators (IL6, IL8, IP-10, Gro-alpha, Gro-beta and MCP-1) in IL4- or IFNgamma-pretreated cells.

Gene_expression (expression) of Gro-alpha

20) Confidence 0.12 Published 2010 Journal Gut Section Body Doc Link 19996325 Disease Relevance 0 Pain Relevance 0

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