Готові списки джерел за темами / CXCL2

Добірка наукової літератури з теми "CXCL2"

Автор: Grafiati
Опубліковано: 6 вересня 2023

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Статті в журналах з теми "CXCL2"

1

Korbecki, Jan, Klaudyna Kojder, Patrycja Kapczuk, Patrycja Kupnicka, Barbara Gawrońska-Szklarz, Izabela Gutowska, Dariusz Chlubek, and Irena Baranowska-Bosiacka. "The Effect of Hypoxia on the Expression of CXC Chemokines and CXC Chemokine Receptors—A Review of Literature." International Journal of Molecular Sciences 22, no. 2 (January 15, 2021): 843. http://dx.doi.org/10.3390/ijms22020843.

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Hypoxia is an integral component of the tumor microenvironment. Either as chronic or cycling hypoxia, it exerts a similar effect on cancer processes by activating hypoxia-inducible factor-1 (HIF-1) and nuclear factor (NF-κB), with cycling hypoxia showing a stronger proinflammatory influence. One of the systems affected by hypoxia is the CXC chemokine system. This paper reviews all available information on hypoxia-induced changes in the expression of all CXC chemokines (CXCL1, CXCL2, CXCL3, CXCL4, CXCL5, CXCL6, CXCL7, CXCL8 (IL-8), CXCL9, CXCL10, CXCL11, CXCL12 (SDF-1), CXCL13, CXCL14, CXCL15, CXCL16, CXCL17) as well as CXC chemokine receptors—CXCR1, CXCR2, CXCR3, CXCR4, CXCR5, CXCR6, CXCR7 and CXCR8. First, we present basic information on the effect of these chemoattractant cytokines on cancer processes. We then discuss the effect of hypoxia-induced changes on CXC chemokine expression on the angiogenesis, lymphangiogenesis and recruitment of various cells to the tumor niche, including myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs), tumor-associated neutrophils (TANs), regulatory T cells (Tregs) and tumor-infiltrating lymphocytes (TILs). Finally, the review summarizes data on the use of drugs targeting the CXC chemokine system in cancer therapies.
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2

Tian, He, Liyu Wang, Yu Liu, Yalong Wang, Yujia Zheng, Tao Fan, Bo Zheng, et al. "Bioinformatics Analyses Reveals a Comprehensive Landscape of CXC Chemokine Family Functions in Non-Small Cell Lung Cancer." BioMed Research International 2021 (January 25, 2021): 1–34. http://dx.doi.org/10.1155/2021/6686158.

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Backgrounds. Lung cancer is a major source of tumor-related death each year with non-small cell lung cancer (NSCLC) being a prevalent subtype. The metastasis from NSCLC to the brain usually imposes many neuron disorders. Previous studies have suggested that communications among cancer cells and interstitial cells are essential in tumorigenesis and are influenced by chemokines. In the tumor microenvironment, CXC chemokines can participate in the shifting of immune cells and manage tumor cell condition, thus affecting the progression of cancer and patient destinies. However, the expression and values of CXC chemokine family in NSCLC have not been systematically illustrated using public databases. Methods. UALCAN, STRING, ONCOMINE, GeneMANIA, cBioPortal, GEPIA, TISIDB, TRRUST, TIMER, Kaplan-Meier Plotter, and R software were utilized in this study. Results. Based on the TIMER and UACLCAN databases, in LUAD patients, the expression levels of CXCL10, CXCL13, and CXCL14 were significantly elevated while the transcriptional levels of CXCL2/3/4/7/12/16 were significantly reduced; in LUSC patients, the expression levels of CXCL6/10/13/14 were significantly elevated while the expression levels of CXCL2/3/4/5/7/11/12/16/17 were significantly reduced. We found remarkable relevance between the pathological stages of LUAD patients and the expressions of CXCL8 (positive) and CXCL17 (negative). Similarly, there are significant correlations between the pathological stages of LUSC patients and the expressions of CXCL1/2/6/17. In LUAD, patients with low expression levels of CXCL1/4/7/8 and patients with high expression levels of CXCL12/14/16 were associated with a significantly better prognosis. But in LUSC, all correlations between chemokines and prognosis are statistically insignificant. Pairwise expression correlation analysis among CXC chemokines shows that there are 7 significant correlations (between CXCL1 and CXCL2, between CXCL1 and CXCL3, between CXCL1 and CXCL8, between CXCL2 and CXCL3, between CXCL4 and CXCL7, between CXCL9 and CXCL10, and between CXCL9 and CXCL11) in LUAD and 4 significant correlations (between CXCL1 and CXCL8, between CXCL2 and CXCL3, between CXCL4 and CXCL7, and between CXCL10 and CXCL11) in LUSC. Significant correlations between the expressions of CXC chemokines and the infiltration of six common types of immune cells were also discovered in both LUAD and LUSC. Conclusions. We provided a comprehensive landscape of the CXC chemokine family in LUAD and LUSC using the bioinformatics method and found differences between LUSC and LUAD in the field of CXC chemokines. Our study may help validate and identify known novel immunotherapeutic targets and prognostic biomarkers.
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3

Korbecki, Jan, Mateusz Bosiacki, Dariusz Chlubek, and Irena Baranowska-Bosiacka. "Bioinformatic Analysis of the CXCR2 Ligands in Cancer Processes." International Journal of Molecular Sciences 24, no. 17 (August 27, 2023): 13287. http://dx.doi.org/10.3390/ijms241713287.

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Анотація:
Human CXCR2 has seven ligands, i.e., CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL7, and CXCL8/IL-8—chemokines with nearly identical properties. However, no available study has compared the contribution of all CXCR2 ligands to cancer progression. That is why, in this study, we conducted a bioinformatic analysis using the GEPIA, UALCAN, and TIMER2.0 databases to investigate the role of CXCR2 ligands in 31 different types of cancer, including glioblastoma, melanoma, and colon, esophageal, gastric, kidney, liver, lung, ovarian, pancreatic, and prostate cancer. We focused on the differences in the regulation of expression (using the Tfsitescan and miRDB databases) and analyzed mutation types in CXCR2 ligand genes in cancers (using the cBioPortal). The data showed that the effect of CXCR2 ligands on prognosis depends on the type of cancer. CXCR2 ligands were associated with EMT, angiogenesis, recruiting neutrophils to the tumor microenvironment, and the count of M1 macrophages. The regulation of the expression of each CXCR2 ligand was different and, thus, each analyzed chemokine may have a different function in cancer processes. Our findings suggest that each type of cancer has a unique pattern of CXCR2 ligand involvement in cancer progression, with each ligand having a unique regulation of expression.
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4

YAMAMOTO, YURIE, KENJI KURODA, TOMOHIRO SERA, ATSUSHI SUGIMOTO, SHUHEI KUSHIYAMA, SADAAKI NISHIMURA, SHINGO TOGANO, et al. "The Clinicopathological Significance of the CXCR2 Ligands, CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL7, and CXCL8 in Gastric Cancer." Anticancer Research 39, no. 12 (December 2019): 6645–52. http://dx.doi.org/10.21873/anticanres.13879.

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5

Mei, Junjie, M. Anna Kowalska, Ning Dai, Yuhong Liu, Kristin Hudock, Samthamby Jeyaseelan, Janet Lee, Susan Guttentag, Mortimer Poncz, and G. Scott Worthen. "Platelet CXCL7 and CXCL4 inhibit chemokine scavenging and improve innate immunity to bacterial infection (P1317)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 63.14. http://dx.doi.org/10.4049/jimmunol.190.supp.63.14.

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Abstract We recently demonstrated the critical role of CXCL5 in chemokine scavenging, neutrophil homeostasis and host defense to bacterial pneumonia. Here we generated Cxcl7-/- mice and found that Cxcl7 deletion also disrupted expression of CXCL4 and CXCL5, but did not affect expression of two other neutrophil chemokines, CXCL1 and CXCL2. Cxcl4, 7, 5 form a conserved genomic locus (14.5 kb in length) in both human and mice, suggesting their importance during evolution. Heparin treatment of blood led to over 10-fold more plasma CXCL4, but comparable plasma CXCL7 as compared to PBS treatment. In addition, the inactive PPBP form of murine CXCL7 showed considerable binding affinity with red cell DARC. We further delineated the role of CXCL7 and CXCL4 by comparing the phenotypes of Cxcl7-/- and Cxcl5-/- mice. CXCL7 and CXCL4 inhibit chemokine scavenging not only in blood, but also in tissues, and platelet-derived CXCL7 is present in alveolar space and peritoneum. In CXCL1- and nebulized LPS-induced acute lung inflammation models, K. pneumoniae pneumonia and bacteremia models, as compared to Cxcl5-/- mice, Cxcl7-/- mice showed attenuated neutrophil chemokine levels in tissues and blood, decreased neutrophil influx to the lung, and impaired innate immunity. This study is the first to reveal the central role of homeostatic CXCL7 and CXCL4 in increasing chemokine levels in blood and tissues, and potentiating neutrophil transmigration during inflammation and infection.
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6

Hong, Jung-Hee, and Young-Cheol Lee. "Anti-Inflammatory Effects of Cicadidae Periostracum Extract and Oleic Acid through Inhibiting Inflammatory Chemokines Using PCR Arrays in LPS-Induced Lung inflammation In Vitro." Life 12, no. 6 (June 8, 2022): 857. http://dx.doi.org/10.3390/life12060857.

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In this study, we aimed to evaluate the anti-inflammatory effects and mechanisms of CP and OA treatments in LPS-stimulated lung epithelial cells on overall chemokines and their receptors using PCR arrays. In addition, we aimed to confirm those effects and mechanisms in LPS-stimulated lung macrophages on some chemokines and cytokines. In our study, CP treatments significantly inhibited the inflammatory mediators CCL2, CCL3, CCL4, CCL5, CCL6, CCL9, CCL11, CCL17, CCL20, CXCL1, CXCL2, CXCL3, CXCL5, CXCL7, CXCL10, TNF-α, and IL-6, while markedly suppressing NF-κB p65 nuclear translocation and the phosphorylations of PI3K p55, Akt, Erk1/2, p38, and NF-κB p65 in LPS-stimulated lung epithelial cells. CP treatments also significantly decreased the inflammatory mediators CCL2, CCL5, CCL17, CXCL1, and CXCL2, while markedly inhibiting phospho-PI3K p55 and iNOS expression in LPS-stimulated lung macrophages. Likewise, OA treatments significantly suppressed the inflammatory mediators CCL2, CCL3, CCL4, CCL5, CCL8, CCL11, CXCL1, CXCL3, CXCL5, CXCL7, CXCL10, CCRL2, TNF-α, and IL-6, while markedly reducing the phosphorylations of PI3K p85, PI3K p55, p38, JNK, and NF-κB p65 in LPS-stimulated lung epithelial cells. Finally, OA treatments significantly inhibited the inflammatory mediators CCL2, CCL5, CCL17, CXCL1, CXCL2, TNF-α, and IL-6, while markedly suppressing phospho-PI3K p55, iNOS, and Cox-2 in LPS-stimulated lung macrophages. These results prove that CP and OA treatments have anti-inflammatory effects on the inflammatory chemokines and cytokines by inhibiting pro-inflammatory mediators, including PI3K, Akt, MAPKs, NF-κB, iNOS, and Cox-2. These findings suggest that CP and OA are potential chemokine-based therapeutic substances for treating the lung and airway inflammation seen in allergic disorders.
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7

Hu, Jing, Qian Ji, Fei Chen, Xiaoqin Gong, Chuansheng Chen, Kaijun Zhang, Ye Hua, et al. "CXCR2 Is Essential for Radiation-Induced Intestinal Injury by Initiating Neutrophil Infiltration." Journal of Immunology Research 2022 (July 16, 2022): 1–9. http://dx.doi.org/10.1155/2022/7966089.

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Neutrophils, known as an important part of the immune system, are the most abundant leukocyte population in peripheral blood, but excessive recruitment will lead to tissue/organ injury. RNA sequencing showed that ionizing radiation significantly increased the expression of characteristic genes of neutrophils in intestinal tissues compared with liver and lung tissues. By clearing neutrophils with an anti-Ly6G antibody, we found that neutrophil infiltration is critical for irradiation-induced intestinal injury. CXCR2 is a G-protein-coupled receptor that mediates the migration of neutrophils by combining with its ligands. Compared with observations in liver and lung tissues, we found that CXCR2 and its ligands, including CXCL1, CXCL2, CXCL3, and CXCL5, were all significantly upregulated in irradiated intestinal tissues. Further studies showed that SB225002, an inhibitor of CXCR2, could effectively inhibit the chemotaxis of neutrophils and tissue damage mediated by the CXCL-CXCR2 signalling pathway.
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8

Situ, Yongli, Xiaoyong Lu, Yongshi Cui, Qinying Xu, Li Deng, Hao Lin, Zheng Shao, and Jv Chen. "Systematic Analysis of CXC Chemokine–Vascular Endothelial Growth Factor A Network in Colonic Adenocarcinoma from the Perspective of Angiogenesis." BioMed Research International 2022 (October 4, 2022): 1–19. http://dx.doi.org/10.1155/2022/5137301.

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Background. Tumor angiogenesis plays a vital role in tumorigenesis, proliferation, and metastasis. Recently, vascular endothelial growth factor A (VEGFA) and CXC chemokines have been shown to play vital roles in angiogenesis. Exploring the expression level, gene regulatory network, prognostic value, and target prediction of the CXC chemokine-VEGFA network in colon adenocarcinoma (COAD) is crucial from the perspective of tumor angiogenesis. Methods. In this study, we analyzed gene expression and regulation, prognostic value, target prediction, and immune infiltrates related to the CXC chemokine-VEGFA network in patients with COAD using multiple databases (cBioPortal, UALCAN, Human Protein Atlas, GeneMANIA, GEPIA, TIMER (version 2.0), TRRUST (version 2), LinkedOmics, and Metascape). Results. Our results showed that CXCL1/2/3/5/6/8/11/16/17 and VEGFA were markedly overexpressed, while CXCL12/13/14 were underexpressed in patients with COAD. Moreover, genetic alterations in the CXC chemokine-VEGFA network found at varying rates in patients with COAD were as follows: CXCL1/2/17 (2.1%), CXCL3/16 (2.6%), CXCL5/14 (2.4%), CXCL6 (3%), CXCL8 (0.8%), CXCL11/13 (1.9%), CXCL12 (0.6%), and VEGFA (1.3%). Promoter methylation of CXCL1/2/3/11/13/17 was considerably lower in patients with COAD, whereas methylation of CXCL5/6/12/14 and VEGFA was considerably higher. Furthermore, CXCL9/10/11 and VEGFA expression was notably correlated with the pathological stages of COAD. In addition, patients with COAD with high CXCL8/11/14 or low VEGFA expression levels survived longer than patients with dissimilar expression levels. CXC chemokines and VEGFA form a complex regulatory network through coexpression, colocalization, and genetic interactions. Moreover, many transcription factor targets of the CXC chemokine-VEGFA network in patients with COAD were identified: RELA, NFKB1, ZFP36, XBP1, HDAC2, SP1, ATF4, EP300, BRCA1, ESR1, HIF1A, EGR1, STAT3, and JUN. We further identified the top three miRNAs involved in regulating each CXC chemokine within the network: miR-518C, miR-369-3P, and miR-448 regulated CXCL1; miR-518C, miR-218, and miR-493 regulated CXCL2; miR-448, miR-369-3P, and miR-221 regulated CXCL3; miR-423 regulated CXCL13; miR-378, miR-381, and miR-210 regulated CXCL14; miR-369-3P, miR-382, and miR-208 regulated CXCL17; miR-486 and miR-199A regulated VEGFA. Furthermore, the CXC chemokine-VEGFA network in patients with COAD was notably associated with immune infiltration. Conclusions. This study revealed that the CXC chemokine-VEGFA network might act as a prognostic biomarker for patients with COAD. Moreover, our study provides new therapeutic targets for COAD, serving as a reference for further research in the future.
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Mu, Li, Shun Hu, Guoping Li, Ping Wu, Caihong Ren, Taiyu Lin, and Sheng Zhang. "Characterization of the Prognostic Values of CXCL Family in Epstein–Barr Virus Associated Gastric Cancer." Oxidative Medicine and Cellular Longevity 2022 (June 1, 2022): 1–24. http://dx.doi.org/10.1155/2022/2218140.

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Анотація:
Background. CXCL family is a class of secreted growth factors signaling through G-protein-coupled receptors, and abnormal expression is associated with the growth and progression of many tumors. However, their prognostic value has been poorly studied in Epstein–Barr virus- (EBV-) associated gastric cancer (EBVaGC). Therefore, it is of great significance to explore the prognostic value of the CXCL family in EBVaGC. Methods. CXCL family mRNA expression was analyzed in STAD data from The Cancer Genome Atlas (TCGA). Kaplan-Meier Plotter was used to assess the prognostic value of the CXCL family. Transcription factors (TFs) and miRNAs associated with the CXCL family were identified by TFCheckpoint, miRWalk, and ViRBase databases. The prognostic model was evaluated using the EBVaGC patient cohort GSE51575. Results. The mRNA expression of CXCL1/3/5/6/8/9/10/11/16 was significantly upregulated, while the expression of CXCL12/14 was downregulated in EBVaGC compared with normal tissues from TCGA-STAD. The mRNA expressions of CXCL9, CXCL10, CXCL11, and CXCL17 in EBVaGCs were higher than those in EBVnGCs, but the mRNA expressions of CXCL6, CXCL12, and CXCL17 were lower than those in EBVnGCs. The mRNA expression levels of CXCL9, CXCL10, and CXCL11 in EBVaGCs were higher than those in EBVnGCs regardless of the tumor stage. High mRNA expression of CXCL8 was associated with better OS in patients with EBVaGC, while high expression of CXCL9 was associated with better OS in patients with EBVnGC. We obtained 10 candidate potential transcription factors (TFs) associated with CXCLs: OTOP3, NKX6-2, NKX2-2, FEV, SMYD1, TRIMSO, TBX10, CDX1, SLC26A3, and ARC. 576 miRNA-mRNA interactions were obtained. Among them, 65 miRNAs were predicted to be correlated with CXCL6, CXCL9, CXCL10, and CXCL11. Similar to the results of TCGA-STAD, the GSE51575 dataset also showed that the mRNA expression levels of CXCL1/3/9/10/11/16 were markedly enhanced in EBVaGC tissues compared with corresponding normal gastric mucosa tissues, while the mRNA expression levels of CXCL12/14 were significantly reduced. The mRNA expression levels of CXCL3/9/10/11/13/17 were increased in EBVaGC compared with EBVnGC tissues. Conclusions. The expression differences of CXCL family members are closely associated with the progression of EBVaGC. Expression of CXCL9/10/11/17 mRNA may be a promising prognostic indicator for EBVaGC patients.
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Sun, Xiaoqi, Qunxi Chen, Lihong Zhang, Jiewei Chen, and Xinke Zhang. "Exploration of prognostic biomarkers and therapeutic targets in the microenvironment of bladder cancer based on CXC chemokines." Mathematical Biosciences and Engineering 18, no. 5 (2021): 6262–87. http://dx.doi.org/10.3934/mbe.2021313.

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<abstract> <sec><title>Background</title><p>Bladder cancer (BLCA) has a high rate of morbidity and mortality, and is considered as one of the most malignant tumors of the urinary system. Tumor cells interact with surrounding interstitial cells, playing a key role in carcinogenesis and progression, which is partly mediated by chemokines. CXC chemokines exert anti-tumor biological roles in the tumor microenvironment and affect patient prognosis. Nevertheless, their expression and prognostic values patients with BLCA remain unclear.</p> </sec> <sec><title>Methods</title><p>We used online tools, including Oncomine, UALCAN, GEPIA, GEO databases, cBioPortal, GeneMANIA, DAVID 6.8, Metascape, TRUST (version 2.0), LinkedOmics, TCGA, and TIMER2.0 to perform the relevant analysis.</p> </sec> <sec><title>Results</title><p>The mRNA levels of C-X-C motif chemokine ligand (<italic>CXCL)1</italic>, <italic>CXCL5</italic>, <italic>CXCL6</italic>, <italic>CXCL7</italic>, <italic>CXCL9</italic>, <italic>CXCL10</italic>, <italic>CXCL11</italic>, <italic>CXCL13</italic>, <italic>CXCL16</italic>, and <italic>CXCL17</italic> were increased significantly increased, and those of <italic>CXCL</italic>2, <italic>CXCL3</italic>, and <italic>CXCL12</italic> were decreased significantly in BLCA tissues as assessed using the Oncomine, TCGA, and GEO databases. GEO showed that high levels of <italic>CXCL1</italic>, <italic>CXCL6</italic>, <italic>CXCL10</italic>, <italic>CXCL1</italic>1, and <italic>CXCL13</italic> mRNA expression are associated significantly with the poor overall survival (all p &lt; 0.05), and similarly, those of <italic>CXCL2</italic> and <italic>CXCL12</italic> in the TCGA database (p &lt; 0.05). The predominant signaling pathways involving the differentially expressed CXC chemokines are cell cycle, chemokine, and cytokine-cytokine receptor interaction. Moreover, transcription factors such as Sp1 transcription factor (SP1), nuclear factor kappa B subunit 1 (NFKB1), and RELA proto-oncogene, NF-KB subunit (RELA) were likely play critical roles in regulating CXC chemokine expression. LYN proto-oncogene, src family tyrosine kinase (LYN) and LCK proto-oncogene, src family tyrosine kinase (LCK) were identified as the key targets of these CXC chemokines. MicroRNAs miR200 and miR30 were identified as the main microRNAs that interact with several CXC chemokines through an miRNA-target network. The expression of these chemokines is closely associated with the infiltration of six categories of immune cells.</p> </sec> <sec><title>Conclusion</title><p>We explored the CXC chemokines superfamily-based biomarkers associated with BLCA prognosis using public databases, and provided possible chemokine targets for patients with BLCA.</p> </sec> </abstract>
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Більше джерел

Дисертації з теми "CXCL2"

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Danilucci, Taís Marolato [UNESP]. "CXCL12 estimula fibroblastos pulmonares a produzir CCL3, CXCL2, LTB4 e LTC4 via p38, MEK1/2, PI-3K e JNK." Universidade Estadual Paulista (UNESP), 2013. http://hdl.handle.net/11449/108908.

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Анотація:
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
A quimiocina C-X-X motif ligand 12 (CXCL12) e seu receptor de quimiocina 4 (CXCR4) desenvolvem um papel crítico na inflamação das vias aéreas. No entanto, os efeitos da ativação da via CXCL12/CXCR4 sobre fibroblastos pulmonares ainda são desconhecidos. Neste estudo, investigamos o efeito da via CXCL12/CXCR4 sobre a quimiocina (C-C motif) ligante 3 (CCL3) e (C-X-C motif) ligante 2 (CXCL2) e sobre os mediadores lipídicos leucotrienos B4 (LTB4) e C4 (LTC4) por fibroblastos pulmonares e a sinalização intracelular envolvida neste processo. CXCL12 foi capaz de induzir a produção de CCL3, CXCL2, LTB4 e LTC4; a produção de CCL3 não é dependente da produção de CXCL2, mas a produção de CXCL2 é dependente da produção de CCL3. A produção de LTB4 pode ser parcialmente regulada por CXCL2 e CCL3 e a produção de LTC4 é dependente da produção de CCL3 e CXCL2. Fibroblastos pulmonares constitutivamente expressam CXCR4 e a estimulação com CXCL12 induz sua expressão. Análises de Western blot mostraram que CXCL12 aumenta a expressão proteica de CXCR4 e induz a fosforilação da S339 do CXCR4. A expressão gênica constitutiva e induzida de CXCR4 foram inibidas pelo anticorpo anti-CXCL2. No entanto, o anticorpo anti-CCL3 e o inibidor farmacológico MK886 foram capazes de diminuir a expressão gênica induzida de CXCR4. Os fibroblastos pulmonares foram pré-tratados com MK886, dexametasona (Dexa) e/ou loratadina (Lor). MK886 e Lor promoveram a diminuição da produção de LTC4 e LTB4, mas não a de CCL3 e CXCL2. Dexa diminuiu níveis de CCL3, CXCL2, LTB4 e LTC4, e quando associado com Lor esta diminuição foi mais eficaz. Identificamos...
C-X-X motif ligand 12 (CXCL12) and its specific receptor Chemokine receptor 4 (CXCR4) play a critical role in airway inflammation. However, the effects of CXCL12/CXCR4 axis on pulmonary fibroblast activation are unknown. In this study, we investigated the effect of CXCL12/CXCR4 axis on chemokine (C-C motif) ligand 3 (CCL3), chemokine (C-X-C motif) ligand 2 (CXCL2), leukotrienes B4 (LTB4) and C4 (LTC4) production by pulmonary fibroblasts and the intracellular signaling involved in the process. CXCL12 induced CCL3, CXCL2, LTB4 and LTC4 production, and CCL3 production is not dependent on CXCL2; but CXCL2 production is dependent on CCL3 production. LTB4 production can be partially down-regulated by CXCL2 and CCL3 production and LTC4 production is dependent on CCL3 and CXCL2 production. Pulmonary fibroblasts constitutively expressed CXCR4, and CXCL12 stimulation up-regulated its expression. Western blot analysis showed that CXCL12 increased protein expression of CXCR4 and induced phosphorylation at S339 of CXCR4. Constitutive CXCR4 expression was decreased by anti-CCL3 antibody or MK 886. Inducible CXCR4 was inhibited by anti-CXCL2 antibody. Indeed pulmonary fibroblasts were pretreated with MK886, dexamethasone (Dexa) and loratadine (Lor). MK886 and loratadine was able to reduced LTB4 and LTC4 production but not CCL3 and CXCL2. Dexa decreased CCL3, CXCL2, LTB4 and LTC4 production, and when associated with Lor this decrease was more effective. We found that PI-3K and JNK intracellular signaling play a role in CCL3 production; p38, MEK1/2, PI-3K and JNK are involved in CXCL2 production and p38 and MEK1/2 pathways are involved in LTB4 production by...
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2

Danilucci, Taís Marolato. "CXCL12 estimula fibroblastos pulmonares a produzir CCL3, CXCL2, LTB4 e LTC4 via p38, MEK1/2, PI-3K e JNK /." Araçatuba, 2013. http://hdl.handle.net/11449/108908.

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Анотація:
Orientador: Sandra Helena Penha de Oliveira
Banca: Edson Antunes
Banca: Lucia Helena Faccioli
Resumo: A quimiocina C-X-X motif ligand 12 (CXCL12) e seu receptor de quimiocina 4 (CXCR4) desenvolvem um papel crítico na inflamação das vias aéreas. No entanto, os efeitos da ativação da via CXCL12/CXCR4 sobre fibroblastos pulmonares ainda são desconhecidos. Neste estudo, investigamos o efeito da via CXCL12/CXCR4 sobre a quimiocina (C-C motif) ligante 3 (CCL3) e (C-X-C motif) ligante 2 (CXCL2) e sobre os mediadores lipídicos leucotrienos B4 (LTB4) e C4 (LTC4) por fibroblastos pulmonares e a sinalização intracelular envolvida neste processo. CXCL12 foi capaz de induzir a produção de CCL3, CXCL2, LTB4 e LTC4; a produção de CCL3 não é dependente da produção de CXCL2, mas a produção de CXCL2 é dependente da produção de CCL3. A produção de LTB4 pode ser parcialmente regulada por CXCL2 e CCL3 e a produção de LTC4 é dependente da produção de CCL3 e CXCL2. Fibroblastos pulmonares constitutivamente expressam CXCR4 e a estimulação com CXCL12 induz sua expressão. Análises de Western blot mostraram que CXCL12 aumenta a expressão proteica de CXCR4 e induz a fosforilação da S339 do CXCR4. A expressão gênica constitutiva e induzida de CXCR4 foram inibidas pelo anticorpo anti-CXCL2. No entanto, o anticorpo anti-CCL3 e o inibidor farmacológico MK886 foram capazes de diminuir a expressão gênica induzida de CXCR4. Os fibroblastos pulmonares foram pré-tratados com MK886, dexametasona (Dexa) e/ou loratadina (Lor). MK886 e Lor promoveram a diminuição da produção de LTC4 e LTB4, mas não a de CCL3 e CXCL2. Dexa diminuiu níveis de CCL3, CXCL2, LTB4 e LTC4, e quando associado com Lor esta diminuição foi mais eficaz. Identificamos...
Abstract: C-X-X motif ligand 12 (CXCL12) and its specific receptor Chemokine receptor 4 (CXCR4) play a critical role in airway inflammation. However, the effects of CXCL12/CXCR4 axis on pulmonary fibroblast activation are unknown. In this study, we investigated the effect of CXCL12/CXCR4 axis on chemokine (C-C motif) ligand 3 (CCL3), chemokine (C-X-C motif) ligand 2 (CXCL2), leukotrienes B4 (LTB4) and C4 (LTC4) production by pulmonary fibroblasts and the intracellular signaling involved in the process. CXCL12 induced CCL3, CXCL2, LTB4 and LTC4 production, and CCL3 production is not dependent on CXCL2; but CXCL2 production is dependent on CCL3 production. LTB4 production can be partially down-regulated by CXCL2 and CCL3 production and LTC4 production is dependent on CCL3 and CXCL2 production. Pulmonary fibroblasts constitutively expressed CXCR4, and CXCL12 stimulation up-regulated its expression. Western blot analysis showed that CXCL12 increased protein expression of CXCR4 and induced phosphorylation at S339 of CXCR4. Constitutive CXCR4 expression was decreased by anti-CCL3 antibody or MK 886. Inducible CXCR4 was inhibited by anti-CXCL2 antibody. Indeed pulmonary fibroblasts were pretreated with MK886, dexamethasone (Dexa) and loratadine (Lor). MK886 and loratadine was able to reduced LTB4 and LTC4 production but not CCL3 and CXCL2. Dexa decreased CCL3, CXCL2, LTB4 and LTC4 production, and when associated with Lor this decrease was more effective. We found that PI-3K and JNK intracellular signaling play a role in CCL3 production; p38, MEK1/2, PI-3K and JNK are involved in CXCL2 production and p38 and MEK1/2 pathways are involved in LTB4 production by...
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Di, Cesare Sebastian 1983. "The characterization of CXCL12, CXCL8, CXCL1 and HGF in five human uveal melanoma cell lines /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112614.

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Uveal Melanoma is the most common primary intraocular tumor in adults. Despite the advances in numerous ophthalmic techniques leading to the increased accuracy of diagnosing this malignancy, the ten-year mortality rate for patients has remained unchanged at approximately fifty percent. Knowing this, further understanding of the specific steps that occur within the metastatic cascade of uveal melanoma is required.
Our laboratory utilizes five human uveal melanoma cell lines (92.1, SP6.5, MKT-BR, OCM-1, UW-1) of known proliferative, invasive, and metastatic potential. We used four methods to characterize the presence and roles of the chemotactic factors CXCL12, CXCL8, CXCL1 and HGF in these five cell lines. We also used a novel peptide inhibitor (TN14003) to block the biological action of CXCL12 on its receptor CXCR4.
With the results obtained from this thesis, we were able to establish the novel presence and importance of the four chosen factors for this malignancy. We were also able to display the positive effects TN14003 had on inhibiting uveal melanoma cell migration in vitro. This may lead to a future therapeutic target, which ultimately may delay or inhibit the metastatic process in uveal melanoma patients, improving the present unaffected ten-year mortality rate.
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Salim, Patrícia Hartstein. "Influência dos polimorfismos genéticos NFKB1, IL-10, CXCR2 E CXCL8 na esclerose sistêmica." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/76191.

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A esclerose sistêmica (ES) é uma doença difusa do tecido conjuntivo caracterizada por anormalidades fibróticas, imunológicas e vasculares. O fator nuclear-kB (NF-kB), como um fator de transcrição essencial envolvido na regulação de respostas imunitárias, parece ser um bom candidato para estudos sobre a patogênese de doenças autoimunes, bem como a interleucina-10 (IL-10) e as quimiocinas, CXCL8 e CXCR2. Vários estudos demonstram o envolvimento dos genes CXCR2 e IL-10 na patogênese das doenças autoimunes. Acredita-se que combinações desses genes possam ser favoráveis para o desenvolvimento da ES, podendo seu conhecimento ser benéfico para o entendimento da patogênese da ES. O objetivo deste estudo é investigar o polimorfismo dos genes IL-10, CXCR2, CXCL8 e NFKB1 em um grupo de pacientes com ES, incluindo a forma difusa e limitada da doença. Nossos resultados confirmam a associação do fenótipo de alta produção (GCC + / GCC +) com risco aumentado para ES, mas não encontrou nenhuma correlação com polimorfismos do NF-KB. Nossos achados também sugerem um papel protetor da CXCL8 (- 251) A nos genótipos TT e TC do gene CXCR2 (+1208) e um risco aumentado do CXCL8 (-251) A em associação com o genótipo CC do CXCR2 (+1208) em pacientes com ES. Nenhuma diferença estatística no polimorfismo dos genes IL-10, CXCR2, CXCL8 e NFKB1 foram encontradas entre a forma difusa e a forma limitada. Estes resultados indicam um potencial papel do gene IL-10 e da combinação CXCR2/CXCL8 na patogênese da ES.
Systemic sclerosis (SSc) is a connective tissue disease characterized by fibrotic, immunological and vascular abnormalities. Nuclear factor-kB (NF-kB), as a key transcription factor involved in the regulation of immune responses, appears to be a good candidate for studies on the pathogenesis of autoimmune diseases, as well as the interleukin-10 (IL-10) polymorphism, and CXCL8 and CXCR2 chemokines. Several studies have demonstrated the involvement of genes CXCR2 and IL-10 in the pathogenesis of autoimmune diseases. It is believed that combinations of these genes may be favorable for the development of SSc, and this knowledge can contribute to the understanding of the pathogenesis of SSc. The objective of this study is to investigate the polymorphism of IL-10, CXCR2, CXCL8 and NFKB1 in a group of patients with SSc, including diffuse and limited subtypes of the disease. Our results confirm the association of high-producing phenotype (GCC/GCC) with increased risk for SSc, but found no correlation with NFKB1 polymorphisms. Our findings also suggest a protective role of CXCL8 (-251) A in the CXCR2 (+1208) TT and TC genotypes and an increased risk of CXCL8 (-251) A in association with the CXCR2 (+1208) CC genotype in SSc patients. No statistical difference in the polymorphism of IL-10, NFKB1, CXCR2 and CXCL8 were found between the diffuse and limited SSc. These results indicate a potential role of the IL-10 gene and the combination CXCR2/CXCL8 in the pathogenesis of SSc.
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Adlard, Nichola Jayne. "Expression of chemokines CXCL4 and CXCL7 in the synovium at an early stage of rheumatoid arthritis." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6600/.

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Identification of suitable biomarkers is growing increasingly important for the treatment of rheumatoid arthritis (RA). They can be measured in a number of different biological materials and can provide clinical information regarding prediction, diagnosis, and prognosis of disease, as well as response to therapeutics. In this thesis, I utilised synovial biopsies collected from patients enrolled in the Birmingham Early Inflammatory Arthritis Cohort (BEACON) to test the hypothesis that detection of expression of CXCL4 and CXCL 7 may be used to predict progression of early stage synovitis to RA. I found that these two chemokines, CXCL4 and CXCL 7, were predominantly expressed on macrophages within the synovium of patients presenting with early synovitis. Increased CXCL4 and CXCL 7 was observed in patients with early RA compared to those with a resolving disease course. However, this increase was transient as expression in treatment naive established RA patients ( > 12 weeks duration, < 3 years duration) was comparable to uninflamed controls. Moreover, I identified expression of a variant ofCXCL4, CXCL4Ll in the rheumatoid synovium. Expression of this potent inhibitor of angiogenesis was evident in the lining layer of the synovium. These data highlight CXCL4 and CXCL 7 as potential predictors of disease outcome in patients presenting with early synovitis.
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Ogawa, Ryotaro. "Loss of SMAD4 Promotes Colorectal Cancer Progression by Recruiting Tumor-Associated Neutrophils via the CXCL1/8-CXCR2 Axis." Kyoto University, 2019. http://hdl.handle.net/2433/245315.

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Denoyer, Alexandre. "Rôle des chimiokines CXCL12 et CXCL1 dans la physiopathologie du trabéculum et de la surface oculaire au cours du glaucome." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2011. http://tel.archives-ouvertes.fr/tel-00824694.

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Le glaucome primitif à angle ouvert est une neuropathie optique rétinienne dont le premier facteur de risque, l'hypertonie intraoculaire, est causé par une dégénérescence du trabéculum dont les mécanismes demeurent inconnus. Ainsi, les traitements actuels ne ciblent pas la trabéculopathie originelle, ce qui pourrait expliquer leur inefficacité parfois observée. En outre, ces traitements contiennent un conservateur, le chlorure de benzalkonium (BAC), qui est responsable d'une inflammation iatrogène de la surface oculaire mise en cause dans l'inobservance thérapeutique. Les chimiokines, cytokines initialement décrites du fait de leurs propriétés chimioattractantes, sont également impliquées dans le contrôle de la viabilité cellulaire et du microenvironnement tissulaire. Dans cette thèse, nous démontrons l'existence d'une balance au niveau trabéculaire entre le système CXCL12/CXCR4 aux effets protecteurs et le système SDF-1(5-67)/CXCR3 proapoptotique. Nous rapportons de façon originale que l'utilisation in vivo d'un antagoniste non-peptidique spécifique de CXCR3 diminue la pression intraoculaire en restaurant la fonction trabéculaire dans un modèle animal de glaucome. En parallèle, nous révélons que les cellules épithéliales conjonctivales exposées au BAC attirent certaines populations leucocytaires via CX3CL1/CX3CR1, montrant ainsi que ce système est impliqué dans le trafic immunitaire au sein de la surface oculaire. De façon originale, les chimiokines apparaissent comme un système inédit de régulation de l'environnement trabéculaire et de la surface oculaire, constituant ainsi de nouvelles cibles thérapeutiques spécifiques
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Mateo, Lou. "Synthèse et évaluation de nouveaux antagonistes des récepteurs CXCR1-2 pour cibler conjointement l’angiogenèse et l’inflammation dans les pathologies cancéreuses." Thesis, Université Côte d'Azur, 2021. http://www.theses.fr/2021COAZ4006.

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L’angiogenèse et l’inflammation sont deux acteurs primordiaux dans le développement et la progression de nombreux cancers. Une meilleure connaissance des mécanismes cellulaires a permis l’essor des thérapies ciblées anti-angiogéniques. L’intérêt de ces thérapies ciblées anti-angiogéniques, est limité du fait de l’apparition de résistances. En parallèle de la voie du VEGF, il existe un second axe pro-angiogénique et pro-inflammatoire : la voie des CXCL-ELR+/CXCR, qui est particulièrement sollicitée dans le cancer et notamment dans le cancer du rein métastatique. Le but de cette thèse a été de développer de petites molécules originales capables d’inhiber l’interaction ligands/récepteurs (CXCL/CXCR1-2) afin d’avoir une action duale : à la fois anti-inflammatoire et anti-angiogénique. Le motif 2-aminobenzothiazinone a été choisi pour la préparation de trois familles d’inhibiteurs. Des stratégies de synthèse divergentes permettent d’obtenir les composés des deux premières familles, bien que les conditions opératoires aient nécessité une adaptation en fonction de la réactivité de chaque substrat. La dernière famille de molécules, est accessible selon une stratégie de synthèse linéaire qui comporte cependant des limitations lors de la dernière étape de cyclisation. Les évaluations biologiques des molécules obtenues ont mis en évidence un composé prometteur possédant une IC50 de 0.6 μM sur la lignée 786-O et inhibant la chimiotaxie des cellules exprimant les récepteurs CXCR1-2. Des études supplémentaires vont être effectuée pour confirmer ces résultats préliminaires encourageants afin d’envisager par la suite une campagne in vivo sur des poissons-zèbres, avec ce composé afin d’étudier sa capacité à entraver l’angiogenèse
Cancer is one of the main causes of death in the world. Angiogenesis and inflammation represent two essential hallmarks in the development and progression of tumors and are essential for the survival of the cancer cells. Better knowledge of cellular mechanisms has enabled the development of targeted anti-angiogenic therapies. However, the emergence of resistance constitutes the main limitation of these current anti-angiogenics targeted therapies, as you may know the anti-VEGF therapies. But in parallel to the VEGF pathway, another crucial pro-angiogenic and pro-inflammatory axis in cancers is required: the CXCL-ELR+/CXCR pathway, particularly in metastatic kidney cancer. The aim of this work was to develop original small organic molecules able to inhibit the ligand/receptor interaction (CXCL-ELR+ / CXCR1-2) in order to have both anti-inflammatory and anti-angiogenic activities. The 2-aminobenzothiazinone pattern was chosen for the preparation of 3 new classes of inhibitors. Divergent synthesis strategies were used to obtain the members of families 1 & 2, although the conditions have been adapted according to the reactivity of each substrate. The last family of molecules was prepared according to a linear synthesis. However, this latter strategy displayed some limitations during the cyclisation step. Thereafter, biological evaluations revealed a promising compound exhibiting an IC50 of 0.6 μM on the 786-O cell line compared with our reference molecule (IC50 = 2 μM). Other result highlighted that this compound also exerted an inhibition of the chemotaxis of cells expressing CXCR1-2 receptors. Further studies on zebrafish are planned with this compound in order to study its ability to interfere with the angiogenesis phenomenon in vivo
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Franz, Juliana Pires Marafon. "Estudo de polimorfismos dos genes CXCR2 e IL-8 em pacientes com câncer de próstata e grupo controle." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/139982.

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A Interleucina 8 (IL-8) é uma quimiocina CXC angiogênica que tem papel importante no desenvolvimento e progressão de vários tumores malignos, incluindo o câncer de próstata (CaP). O polimorfismo de nucleotídeo único (SNP) -251 T/A da região promotora do gene da IL-8, relativo ao local de início da transcrição deste gene, está associado com a produção desta citocina. O efeito da IL-8 é mediado através de dois receptores de alta afinidade, CXCR1 e CXCR2. O presente estudo investigou a influência da variação dos genes IL-8 e CXCR2 na susceptibilidade e nas características clinicopatológicas do CaP em um grupo de brasileiros. Duzentos e um pacientes e 185 controles saudáveis foram selecionados neste estudo casocontrole. Amostras de sangue foram coletadas para extração de DNA; a tipagem da IL-8 -251 T/A e CXCR2 +1208 C/T foi realizada através da reação em cadeia da polimerase com sequência específica de primers (PCR-SSP), seguida pela eletroforese em gel de agarose. O risco associado entre os genótipos, a susceptibilidade do CaP e as características do tumor, foi estimado pelo odds ratio (OR), com intervalo de confiança de 95%, usando análise de regressão logística e ajustando para idade ao diagnóstico. Encontramos uma associação estatisticamente significativa entre o genótipo heterozigoto CT do gene CXCR2 +1208 e CaP. Este genótipo foi significativamente menos frequente em pacientes com estádio clínico T3-T4 comparado com T1-T2 (56.7% versus 80.5%). Nossos achados sugerem que os portadores do genótipo CT CXCR2 +1208 tiveram um efeito protetor para estádio avançado de CaP (CT versus CC: OR ajustado = 0.25; P = 0.02). Não foi encontrada associação significativa entre o polimorfismo -251 T/A da IL-8 e os parâmetros clinicopatológicos do CaP. Estes resultados indicam que o genótipo CT do CXCR2 +1208 é menos frequente em estádios avançado de CaP, sugerindo que este receptor de quimiocina tenha um papel na patogênese desta doença.
Interleukin-8 (IL-8) is an angiogenic CXC chemokine that plays an important role in both the development and progression of several human malignancies including prostate cancer (PC). A single nucleotide polymorphism (SNP) at -251 upstream of the transcriptional start site of the IL-8 gene has been shown to influence its production. The effects of IL-8 are mediated by two highly related chemokine receptors, CXCR1 and CXCR2. The present study investigated the influence of the IL-8 and CXCR2 gene variation on susceptibility and clinicopathological characteristics of PC in a group of Brazilian subjects. Two hundred and one patients and 185 healthy controls were enrolled in a case-control study. Blood was collected for DNA extraction; typing of IL-8 -251 T/A and CXCR2 +1208 C/T genes was performed by polymerase chain reaction with sequence-specific primers (PCR-SSP), followed by agarose gel electrophoresis. Risk association between the genotypes, PC susceptibility and tumor characteristics was estimated by odds ratio (OR) and 95% confidence intervals (95% CI) using logistic regression analysis, after adjusting for age at diagnosis. A significant association was found between the heterozygous CXCR2 +1208 CT genotype and PC. The CXCR2 +1208 CT genotype was significantly less frequent in patients with clinical stage T3-T4 compared to T1-T2 (56.7 versus 80.5%). Our findings suggest that carriers of the CXCR2 +1208 CT genotype had a protective effect for advanced PC (CT versus CC: adjusted OR = 0.25; P = 0.02). No association was observed between the SNP for IL-8 -251 T/A and clinicopathological parameters of PC. These results indicated that the CXCR2 +1208 CT genotype is less frequent in advanced stages of PC, suggesting that this chemokine receptor plays a role in the pathogenesis of this disease.
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Desurmont, Thibault. "Etude de l'implication des chimiokines et de leurs récepteurs dans la survenue d'une rechute métastatique chez des patients atteints d'un cancer du côlon métastatique et traités par chirurgie hépatique avec ou sans chimiothérapie néoadjuvante." Thesis, Lille 2, 2015. http://www.theses.fr/2015LIL2S042/document.

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Notre objectif était d’analyser l’implication potentielle des voies associées aux récepteurs de chimiokines CXCR2 et CXCR4 dans le cancer colorectal métastatique au foie. Les niveaux d’expression de CXCR2, CXCR4 et de leurs chimiokines étaient évalués dans les métastases hépatiques de cancers colorectaux dans le but d’étudier leurs corrélations avec la survie globale et la survie sans récidive de patients ayant reçu, ou non, une chimiothérapie néoadjuvante. Des analyses d’expression pour RT-PCR quantitative et immunohistochimie étaient réalisées en utilisant des prélèvements humains de métastases hépatiques de cancers colorectaux. Les niveaux d’expression de CXCR2, CXCR4 et de leurs ligands étaient statistiquement analysés en fonction des traitements par chimiothérapie néoadjuvante administrés ou non, et en fonction du suivi des patients. Des modèles murins de xénogreffes sous-cutanées et orthotopiques intracaecales ont été mis au point et utilisés pour étudier l’expression de CXCR2, CXCR4 et CXCL7 en relation avec le traitement des souris par chimiothérapie.Nous avons montré que la surexpression de CXCR2 et CXCL7 était corrélée à de plus courtes survies globales et sans récidive de nos patients. En analyse multivariée, l’expression de CXCR2 et de CXCL7 étaient des facteurs indépendants de survie globale et sans récidive. La chimiothérapie néoadjuvante augmentait significativement l’expression de CXCR2, et de CXCL7 de façon proche de la significativité. Les résultats de nos modèles murins ont montré une tendance à la surexpression de nos gènes d’intérêts dans les tissus tumoraux des souris traités. En conclusion, ces résultats suggèrent l’implication de la voie de signalisation CXCL7/CXCR2 comme facteur prédictif de mauvais pronostic dans le cancer colorectal métastatique. Les chimiothérapies à base de 5 Fluoro-uracile augmentent l’expression de ces gènes dans les métastases hépatiques, fournissant une explication sur l’agressivité des tumeurs métastatiques en échappement thérapeutique. Un blocage sélectif de l’axe CXCR2/CXL7 pourrait fournir de nouvelles opportunités thérapeutiques
Our aim was to analyze the potential role of chemokine receptors CXCR2 and CXCR4 signalling pathways in liver metastatic colorectal cancer (CRC) relapse. Expression levels of CXCR2, CXCR4, and their chemokine ligands were evaluated in liver metastases of colorectal cancer in order to study their correlation with overall and disease-free survival of patients having received, or not received, a neoadjuvant chemotherapy regimen.Quantitative RT-PCR and CXCR2 immunohistochemical staining were carried out using human CRC liver metastasis samples. Expression levels of CXCR2, CXCR4, and their ligands were statistically analyzed according to treatment with neoadjuvant chemotherapy and patients ' outcome. Murine models of subcutaneous and orthotopic intracaecal xenografts have been developed and used to study the expression of CXCR2, CXCR4 and CXCL7 in connection with the treatment of mice with chemotherapy.We showed that CXCR2 and CXCL7 overexpression are correlated to patient’s shorter overall and disease-free survival. By multivariate analysis, CXCR2 and CXCL7 expressions are independent factors of overall and disease-free survival. Neoadjuvant chemotherapy increases significantly the expression of CXCR2 and CXCL7 was overexpressed close to significance. Results of our mouse models have shown a trend over-expression of our interest genes in tumor tissues of the treated mice.In conclusion, we show the involvement of CXCL7/CXCR2 signalling pathways as a predictive factor of poor outcome in metastatic CRC. 5-Fluorouracil-based chemotherapy regimens increase the expression of these genes in liver metastasis, providing one explanation for aggressiveness of relapsed drug-resistant tumors. Selective blockage of CXCR2/CXCL7 signalling pathways could provide new potential therapeutic opportunities
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Книги з теми "CXCL2"

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Abed, Majed. Role of phosphatidylserine and CXCL-16 in adhesion of erythrocytes to endothelial cells. [S.l: s.n.], 2013.

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Ramjeesingh, Ravi Avinash. Mechanism of CXCL8-mediated chemotaxis during transendothelial migration of melanoma cells. 2005.

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Частини книг з теми "CXCL2"

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Gleissner, Christian A. "CXCL4 und CXCL4L1." In Compendium of Inflammatory Diseases, 389–94. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_13.

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Gleissner, Christian A. "CXCL4 und CXCL4L1." In Encyclopedia of Inflammatory Diseases, 1–7. Basel: Springer Basel, 2015. http://dx.doi.org/10.1007/978-3-0348-0620-6_13-1.

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Moepps, Barbara. "CXCR1 and CXCR2 and Ligands." In Compendium of Inflammatory Diseases, 394–404. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_223.

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Sugita, Yasuo. "Glioblastomas: Role of CXCL12 Chemokine." In Tumors of the Central Nervous System, Volume 1, 137–46. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0344-5_15.

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Moepps, Barbara. "CXCR1 and CXCR2 and Ligands." In Encyclopedia of Inflammatory Diseases, 1–10. Basel: Springer Basel, 2015. http://dx.doi.org/10.1007/978-3-0348-0620-6_223-1.

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Sarau, Henry M., Katherine L. Widdowson, Michael R. Palovich, John R. White, David C. Underwood/surname, and Don E. Griswold. "Interleukin-8 Receptor (CXCR2) Antagonists." In New Drugs for Asthma, Allergy and COPD, 293–96. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000062157.

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Li, Yanchun, and Amy M. Fulton. "The CXCR3/CXCL3 Axis in Cancer." In Chemokine Receptors in Cancer, 79–91. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-267-4_5.

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Uy, Geoffrey L., and John F. DiPersio. "CXCR4/CXCL12 as a Therapeutic Target." In Targeted Therapy of Acute Myeloid Leukemia, 607–15. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_31.

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Reyes, Niradiz, Stephanie Figueroa, Raj Tiwari, and Jan Geliebter. "CXCL3 Signaling in the Tumor Microenvironment." In Advances in Experimental Medicine and Biology, 15–24. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62658-7_2.

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Asokan, Sahana, and Obul Reddy Bandapalli. "CXCL8 Signaling in the Tumor Microenvironment." In Advances in Experimental Medicine and Biology, 25–39. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62658-7_3.

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Тези доповідей конференцій з теми "CXCL2"

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Yamamoto, Yurie, Kenji Kuroda, Tomohiro Sera, Atsushi Sugimoto, Syuhei Kushiyama, Sadaaki Nishimura, Shingo Togano, et al. "Abstract 6193: The clinicopathologic significance of the CXCR2 ligands, CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL7, and CXCL8 in gastric cancer." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-6193.

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Hardaway, Aimalie L., Mackenzie M. Herroon, Erandi N. Rajagurubandara, and Izabela Podgorski. "Abstract 1428: Bone marrow adipocyte-derived CXCL1 and CXCL2 in prostate tumor progression in bone." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1428.

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Wang, C., P. Xu, G. Wang, H. Wang, Y. Zhang, T. Billiar, and J. Zhang. "TLR4 KO MSC optimized protection in liver IRI via CXCR2/CXCL2-mediated crosstalk with Kupffer cells." In 37. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0040-1722087.

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Wan, Shao-Gui, Cristian Taccioli, Hongping Chen, Yubao Jiang, Xiu-Ping Liu, Carlo M. Croce, John L. Farber, and Louise Y. Y. Fong. "Abstract 4174: Cxcl5 and Cxcl2 overexpression in esophageal carcinogenesis is associated with rapid tumor formation in zinc-deficient rats." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4174.

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Jiang, Sisi, Evangeline Mose, Giovanni Coppola, Andrew Lowy, Christina Jamieson, and Nicholas A. Cacalano. "Abstract 4208: Suppressor of Cytokine Signaling (SOCS)-3 and the C-X-C chemokines CXCL1 and CXCL2 promote tumor aggessiveness and radiation resistance in pancreatic cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4208.

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Jiang, Sisi, Giovanni Coppola, Evangeline Mose, Andrew Lowy, Christina Jamieson, and Nicholas Cacalano. "Abstract A10: Suppressor of cytokine signaling (SOCS)-3 and the C-X-C chemokines CXCL1 and CXCL2 promote tumor aggressiveness and radiation resistance in pancreatic cancer." In Abstracts: AACR Special Conference: The Translational Impact of Model Organisms in Cancer; November 5-8, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1557-3125.modorg-a10.

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Yu, Minghuan, and Mary A. Kosir. "Abstract 5276: CXCL7/CXCR2 axis and invasion." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5276.

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Rozycki, Henry J., Adam Brock, Melissa Yopp, Christopher Corday, Shauna Webb-Parker, and Tsuyoshi Tanabe. "Increased CXCL2 Production From Mouse Type II Alveolar Epithelial Cells In Response To The Alarmin HMGB1." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4269.

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Yamamoto, Yurie, Gen Tsujio, Tomohiro Sera, Atsushi Sugimoto, Syuhei Kushiyama, Sadaaki Nishimura, Kenji Kuroda, et al. "Abstract 2677: Clinicopathologic significance of CXCR2-CXCL1 signaling in cholangiocarcinoma." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2677.

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Kuddus, Ruhul H., Asmahan A. El Ezzi, Mohammed A. El-Saidi, Scott Baker, and Wissam Zaidan. "Abstract 4821: Association of polymorphisms in TP53, CXCL2, MDM2, MDM4 and BCL2 genes and proliferative prostate diseases among Lebanese men." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4821.

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Звіти організацій з теми "CXCL2"

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Luker, Gary D. Imaging CXCL12-CXCR4 Regulation of Breast Cancer Metastases. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada433943.

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Luker, Gary D. Imaging CXCL12-CXCR4 Signaling and Inhibition in Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada566816.

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Luker, Gary D. Imaging CXCL12-CXCR4 Signaling and Inhibition in Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada574795.

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Macoska, Jill A. CXCL5 is a Novel Mediator of Prostate Cancer Proliferation and Migration/Invasion. Fort Belvoir, VA: Defense Technical Information Center, June 2008. http://dx.doi.org/10.21236/ada486771.

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