The CXCL8-CXCR1/2 pathways in cancer

Liu, Qian; Li, An‐Ping; Tian, Yijun; Wu, Jennifer D.; Liu, Yu; Li, Tengfei; Chen, Yuan; Han, Xinwei; Wu, Zeyu

doi:10.1016/j.cytogfr.2016.08.002

Cited by 496 publications

(452 citation statements)

References 146 publications

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“…CXCL8 takes a function with its cognate receptors C-X-C chemokine receptor 1 (CXCR1) and CXCR2 14,15. CXCL1 and CXCR2 show increased expression in gastric cancer tissues compared with adjacent noncancerous tissues, and CXCL1 or CXCR2 depletion significantly reduced the migration and invasion ability 16.…”

Section: Discussionmentioning

confidence: 99%

Investigating the expression, effect and tumorigenic pathway of PADI2 in tumors

Guo¹,

Zheng²,

Xu³

et al. 2017

OTT

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BackgroundPeptidylarginine deiminase (PAD) catalyzes the conversion of arginine residues to citrulline residues, termed citrullination. Recent studies have suggested that PAD isoform 2 (PADI2) plays an important role in tumors, although its tumorigenic effect and mechanism are largely unknown.Materials and methodsImmunohistochemistry and enzyme-linked immunosorbent assay (ELISA) were used to investigate the expression level of PADI2 in various tumor tissues and patient blood samples, respectively. MNK-45 and Bel-7402 tumor cell lines originating from gastric and liver tumors, respectively, were treated with anti-PADI2 siRNA, and the subsequent cell proliferation, apoptosis and migration were observed. Polymerase chain reaction (PCR) arrays, including Cancer PathwayFinder, Oncogenes and Tumor Suppressor Genes, p53 Signaling Pathway, Signal Transduction Pathway and Tumor Metastasis PCR arrays, were used to investigate the tumorigenic pathway of PADI2 in the siRNA-treated tumor cells. This analysis was verified by real-time PCR.ResultsImmunohistochemistry detected significantly increased expression of PADI2 in invasive breast ductal carcinoma, cervical squamous cell carcinoma, colon adenocarcinoma, liver hepatocellular carcinoma, lung cancer, ovarian serous papillary adenocarcinoma and papillary thyroid carcinoma samples. ELISA detected a twofold increase in PADI2 expression in the blood of 48.3% of patients with liver cancer, 38% of patients with cervical carcinoma and 32% of patients with gastric carcinoma. Increased apoptosis and decreased cell proliferation and migration were observed in the anti-PADI2 siRNA-treated MNK-45 cells, and increased cell proliferation and migration and decreased apoptosis were observed in the treated Bel-7402 cells with suppressed PADI2 expression. PCR arrays and real-time PCR detected significantly decreased CXCR2 and EPO expression in the MNK-45 cells and Bel-7402 cells, respectively, with the anti-PADI2 siRNA treatments.ConclusionPADI2 expression is increased in many types of tumor tissues and patient blood samples. PADI2 may advance abnormal cell behavior in gastric cancers by mediating CXCR2, a well-known gene that stimulates cell proliferation and invasion. However, PADI2 might have deleterious effects on tumor growth and metastasis in liver tumor cells by regulating the expression of EPO, a gene with controversial functions in tumor growth. The results suggest that the effect of PADI2 on tumorigenesis is multifactorial, depending on the tumor type.

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Section: Discussionmentioning

confidence: 99%

Investigating the expression, effect and tumorigenic pathway of PADI2 in tumors

Guo¹,

Zheng²,

Xu³

et al. 2017

OTT

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“…This chemokine, which is induced by proinflammatory cytokines such as TNFa and IL-1b, recruits neutrophils and granulocytes to sites of inflammation. 59 F8A1, which is nested within the largest intron of factor VIII, is transcribed in the opposite direction of the parent gene. 60 Although its function is unknown, it is interesting to speculate about an involvement in coagulation.…”

Section: Gsta3mentioning

confidence: 99%

Preeclampsia: novel insights from global RNA profiling of trophoblast subpopulations

Gormley

Ona

Kapidzic

et al. 2017

American Journal of Obstetrics and Gynecology

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BACKGROUND:The maternal signs of preeclampsia, which include the new onset of high blood pressure, can occur because of faulty placentation. We theorized that transcriptomic analyses of trophoblast subpopulations in situ would lend new insights into the role of these cells in preeclampsia pathogenesis. OBJECTIVE: Our goal was to enrich syncytiotrophoblasts, invasive cytotrophoblasts, or endovascular cytotrophoblasts from the placentas of severe preeclampsia cases. Total RNA was subjected to global transcriptional profiling to identify RNAs that were misexpressed compared with controls. STUDY DESIGN: This was a cross-sectional analysis of placentas from women who had been diagnosed with severe preeclampsia. Gestational age-matched controls were placentas from women who had a preterm birth with no signs of infection. Laser microdissection enabled enrichment of syncytiotrophoblasts, invasive cytotrophoblasts, or endovascular cytotrophoblasts. After RNA isolation, a microarray approach was used for global transcriptional profiling. Immunolocalization identified changes in messenger RNA expression that carried over to the protein level. Differential expression of noneprotein-coding RNAs was confirmed by in situ hybridization. A 2-way analysis of variance of non-coding RNA expression identified particular classes that distinguished trophoblasts in cases vs controls. Cajal body foci were visualized by coilin immunolocalization. RESULTS: Comparison of the trophoblast subtype data within each group (severe preeclampsia or noninfected preterm birth) identified many highly differentially expressed genes. They included molecules that are known to be expressed by each subpopulation, which is evidence that the method worked. Genes that were expressed differentially between the 2 groups, in a cell-typeespecific manner, encoded a combination of molecules that previous studies associated with severe preeclampsia and those that were not known to be dysregulated in this pregnancy

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“…An enhancing effect of IL-22 on TNF-α or IL-1-stimulated CXCL8 responses could lead to increased neutrophil migration into inflamed mucosal tissues in diseases like IBD, thus exacerbating the detrimental inflammation. However, a role for CXCL8 in wound healing responses exists in that CXCL8 can enhance angiogenesis in several tissues and cancer [24]. Thus, a CXCL8-enhanced angiogenic effect would be consistent with the wound healing aspects of IL-22.…”

Section: Discussionmentioning

confidence: 96%

IL-22 Enhances TNF-α- and IL-1-Induced CXCL8 Responses by Intestinal Epithelial Cell Lines

2017

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IL-22 is known to induce intestinal epithelial cells (IECs) to produce the chemokine CXCL8. However, IECs exist in a cytokine network during mucosal inflammation, such that IL-22 must act in concert with potent pro-inflammatory cytokines like TNF-α and IL-1. Our studies show that IL-22 alone increased CXCL8 secretion from HT-29 cells, but the levels were minimal compared to that of the cells treated with TNF-α or IL-1 only. More significantly, costimulation with IL-22 and TNF-α enhanced both CXCL8 secretion and mRNA levels well over that of TNF-α stimulation alone. A similar enhancing effect was seen with IL-22 and IL-1-stimulated CXCL8 secretion. The enhancing effect of IL-22 on TNF-α-induced CXCL8 secretion was then determined to require the p38 MAPK, but not STAT1/3, PI3K, Akt, JNK, ERK or IкBα. These experiments indicate that the more significant effect of IL-22 on IECs responses may not be in inducing CXCL8 by itself, but of enhancing TNF-α- and IL-1-induced CXCL8 secretion to augment the contribution of IECs to local inflammatory responses.

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The CXCL8-CXCR1/2 pathways in cancer

Cited by 496 publications

References 146 publications

Investigating the expression, effect and tumorigenic pathway of PADI2 in tumors

Investigating the expression, effect and tumorigenic pathway of PADI2 in tumors

Preeclampsia: novel insights from global RNA profiling of trophoblast subpopulations

IL-22 Enhances TNF-α- and IL-1-Induced CXCL8 Responses by Intestinal Epithelial Cell Lines

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