Transfection of interleukin-8 increases angiogenesis and tumorigenesis of human gastric carcinoma cells in nude mice

Kitadai, Yasuhiko; Haruma, Ken; Naka, Kazuhito; Sumii, Koji; Yokozaki, Hiroshi; Yasui, Wataru; Mukaida, Naofumi; Ohmoto, Yasukazu; Kajiyama, Goro; Fidler, Isaiah J.; Tahara, Eiichi

doi:10.1038/sj.bjc.6690742

Cited by 150 publications

(112 citation statements)

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“…CXCL8 can induce human gastric cancer cell lines, which possess CXCR1 and Mukaida 6 CXCR2, to express epidermal growth factor (EGF) receptor, matrix metalloproteinase (MMP)-9, and vascular endothelial growth factor (VEGF) [20]. The same pathway is utilized to promote proliferation of esophageal cancer cells [21] and melanoma cells [22].…”

Section: Direct Effects On Cancer Cellsmentioning

confidence: 99%

Chemokines in tumor development and progression

Mukaida

Baba

2012

Experimental Cell Research

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Section: Direct Effects On Cancer Cellsmentioning

confidence: 99%

Chemokines in tumor development and progression

Mukaida

Baba

2012

Experimental Cell Research

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“…[1][2][3] The expression of multiple factors with proangiogenic activity by cancer cells poses a significant obstacle to effective therapy with agents targeted toward individual factors and receptors. Identification of common mechanism(s) underlying expression of such a diversity of factors could guide the development of therapy using fewer selective agents.…”

mentioning

confidence: 99%

Effects of pharmacologic antagonists of epidermal growth factor receptor, PI3K and MEK signal kinases on NF‐κB and AP‐1 activation and IL‐8 and VEGF expression in human head and neck squamous cell carcinoma lines

Bancroft

Chen

Yeh

et al. 2002

Intl Journal of Cancer

220

190

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Key words: EGFR; NF-B; AP-1; IL-8; VEGF; PI3K; MEK; HNSCCIncreased angiogenesis is critical to tumor progression and metastasis, and we and others have shown that expression of members of the C-X-C cytokine and vascular endothelial growth factor families such as IL-8, growth regulated oncogene-1 (Gro 1) and VEGF can promote angiogenesis, tumorigenesis and metastatic tumor progression. 1-3 The expression of multiple factors with proangiogenic activity by cancer cells poses a significant obstacle to effective therapy with agents targeted toward individual factors and receptors. Identification of common mechanism(s) underlying expression of such a diversity of factors could guide the development of therapy using fewer selective agents. We previously observed that IL-8, VEGF and other cytokines are coexpressed and often vary concurrently in serum and supernatants from cell lines from different patients with head and neck squamous cell carcinoma (HNSCC), 4,5 suggesting that these factors could be regulated by common signal pathways or transcription factors.Examination of the regulatory region of many proinflammatory cytokines and proangiogenic factors reveals that they share common promoter sites for transcription factors such as nuclear factor-B (NF-B) and/or activator protein-1 (AP-1), which can be activated by injury, cytokines and growth factors. 6 We found that differences in expression of these cytokines in different cancers was often related to differences in constitutive activation of both NF-B and AP-1. 6 Inhibition of NF-B activation by expression of a dominant negative inhibitor-B or pharmacologic agents was found to inhibit expression of IL-8 and other proinflammatory and proangiogenic cytokines, 7-10 as well as tumorigenesis and angiogenesis in vivo. 7,9 Inhibition of activation of extracellular signalregulated kinase (ERK) and AP-1 with antagonists of mitogenactivated/extracellular signal-regulated kinase (MEK) partially inhibited expression of both IL-8 and VEGF. 10 These results provided evidence that at least 2 signal pathways upstream of NF-B and AP-1 make important contributions to expression of these angiogenesis factors.We have recently examined the contribution of several factors that may contribute to upstream signal activation of NF-B and AP-1 and expression of IL-8 and VEGF. We found that IL-1␣ expressed by HNSCC promotes autocrine activation of NF-B and AP-1, expression of IL-8 and cell survival. 11 Expression of IL-1 receptor antagonist inhibited NF-B reporter activity and IL-8 expression by 60 -80%, indicating that IL-1␣ is a major contributor to constitutive activation of NF-B and IL-8. HNSCC were also found to express c-MET, a receptor tyrosine kinase for hepatocyte growth factor/scatter factor (HGF/SF). 12 Increased expression of HGF/SF was detected together with IL-8 and VEGF in serum of patients with HNSCC, and recombinant HGF and HGF from stromal fibroblasts was found to further induce IL-8 and VEGF expression by human HNSCC lines. Inhibitors of MEK and Abbreviations: AP-1, activator...

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“…It plays a key role in the maturation of T-helper cells to the Th2 phenotype; with a shift from a Th1 to Th2 cell pattern, it can enhance the production of anti-inflammatory cytokines and inhibit the production of monocyte-derived pro-inflammatory cytokines including IL-8 (Sugimoto et al, 2010). IL-8 enhances cell proliferation and migration, and acts like a chemoattractant for neutrophils and leukocytes, and a proangiogenic factor and mediator of chronic inflammatory processes (Kitadai et al, 1999). It is involved in adhesion, migration, and invasion in human GC cells in vitro (Ju et al, 2012) and highly expressed in GC cells (Xue et al, 2012), and increased IL-8 level may promote the inflammatory response that leads to risk of GC (Sugimoto et al, 2010).…”

Section: Introductionmentioning

confidence: 99%