IL-18 enhances SCF production of melanoma cells by regulating ROI and p38 MAPK activity

Hue, Jeongsim; Kim, Ankeun; Song, Han-Jung; Choi, Inpo; Park, Hyun-Jeong; Kim, Taesung; Lee, Wang Jae; Kang, Hyung‐Sik; Cho, Daeho

doi:10.1016/j.imlet.2004.08.008

Cited by 22 publications

(17 citation statements)

References 38 publications

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“…In contrast, IL-18 inhibits tumor growth by suppressing angiogenesis (55). IL-18 induces melanoma cell proliferation via induction of stem cell factor (45). In the present study we demonstrated that IL-18 induces SMC proliferation in a CXCL16-dependent manner.…”

Section: Fig 8 Il-18 Induced P38 Mapk Erk and Jnk Activation In Asupporting

confidence: 52%

The Pro-atherogenic Cytokine Interleukin-18 Induces CXCL16 Expression in Rat Aortic Smooth Muscle Cells via MyD88, Interleukin-1 Receptor-associated Kinase, Tumor Necrosis Factor Receptor-associated Factor 6, c-Src, Phosphatidylinositol 3-Kinase, Akt, c-Jun N-terminal Kinase, and Activator Protein-1 Signaling

Chandrasekar

Mummidi²,

Valente

et al. 2005

Journal of Biological Chemistry

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Section: Fig 8 Il-18 Induced P38 Mapk Erk and Jnk Activation In Asupporting

confidence: 52%

The Pro-atherogenic Cytokine Interleukin-18 Induces CXCL16 Expression in Rat Aortic Smooth Muscle Cells via MyD88, Interleukin-1 Receptor-associated Kinase, Tumor Necrosis Factor Receptor-associated Factor 6, c-Src, Phosphatidylinositol 3-Kinase, Akt, c-Jun N-terminal Kinase, and Activator Protein-1 Signaling

Chandrasekar

Mummidi²,

Valente

et al. 2005

Journal of Biological Chemistry

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“…The tumor-associated inflammatory cytokines, such as IL-1␤, TNF␣, and IL-18, can enhance SCF secretion by tumor cells, 41,[43][44][45] and thereby further stimulate expansion of MDSCs. VEGF signaling through VEGFR-2 has been shown to promote myelopoiesis and accumulation of MDSCs 46,47 through GM-CSFdependent and -independent mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Reversion of immune tolerance in advanced malignancy: modulation of myeloid-derived suppressor cell development by blockade of stem-cell factor function

Pan

Wang²,

Yin³

et al. 2008

Blood

289

224

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IntroductionImmune-based therapy has achieved a certain level of success; however, the overall therapeutic effect has been much less promising due to the immune suppressive mechanisms associated with advanced malignancies. 1 To achieve a better therapeutic efficacy of immune activation therapy, the mechanism or mechanisms by which a large tumor burden prevents immune activation from inducing effective antitumor immunity needs to be elucidated.Tumor growth is accompanied by an increase in the number of Gr-1 ϩ Mac-1 ϩ myeloid-derived suppressor cells (MDSCs) 2-4 and tumor-specific T regulatory cells (Tregs) 5,6 with strong immune suppressive activity in cancer patients and in tumor-bearing mice. [7][8][9] Both MDSCs and Tregs may be directly involved in immune unresponsiveness in active immune therapy.It has been demonstrated that MDSCs are involved in T-cell hyporesponsiveness in tumor-bearing mice. Several mechanisms by which MDSCs regulate the tumor-specific T-cell response have recently been proposed and the in vivo immune regulatory effects of MDSCs on tumor-specific T-cell response have been identified. 7-12 T-cell inactivation can be mediated by MDSCs through IFN␥-dependent nitric oxide (NO) production [12][13][14][15][16] or the Th2-mediated IL-4/IL-13-dependent arginase 1 pathway. 14,[17][18][19][20][21][22] In addition, a mechanism of ROS-mediated cell killing has been proposed. 3,23,24 Furthermore, MDSCs can inhibit cytotoxic T lymphocyte (CTL) responses through NOdependent or -independent mechanisms. Cell-to-cell contact appeared to be crucial in these mechanisms. 25 Our laboratory has further identified a novel mechanism of MDSC-mediated immune suppression on activated T cells through the development of Foxp3 ϩ T regulatory cells (Tregs) and T-cell tolerance both in vitro and in tumor-bearing mice. The induction of Tregs by MDSCs requires IFN-␥ and IL-10 but is independent of the NO-mediated suppressive mechanism. 11 To overcome MDSCmediated immune suppression and prevent Treg induction, it is critical to identify the tumor factors that are required for MDSC accumulation in tumor-bearing animals.Several lines of evidence support the hypothesis that the development and expansion of MDSCs may be modulated by tumor-secreted factors. MDSCs in tumor-bearing animals can differentiate into mature dendritic cells or remain as MDSCs with inhibitory activities, depending on the local cytokine milieu. 26,27 Human renal cell carcinoma cell lines release soluble factors (IL-6, M-CSF) that inhibit the differentiation of CD34 ϩ cells into dendritic cells (DCs) and trigger their commitment toward monocytic cells. 28 In a transgenic mammary tumor, VEGF levels correlate with the MDSC number. 29 Moreover, the in vivo infusion of vascular endothelial growth factor (VEGF) can induce MDSC development in naive mice and impair DC function and differentiation. 30 Granulocyte macrophage-colony-stimulating factor (GM-CSF) secretion has correlated with the capacity of tumor metastases and the GM-CSF and IL-3 in conditioned mediu...

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“…The MAP kinase signalling pathway is important for controlling various cellular functions such as growth and migration (Widmann et al, 1999;Kampen et al, 2000). The ERK1/2 MAP kinase pathway is constitutively activated in most melanoma cells, where it plays a major role in mediating their survival and proliferation (Hue et al, 2005). The importance of ERK1/2 activation in melanoma progression has also been reported (Zhuang et al, 2005).…”

Section: Schraufstattermentioning

confidence: 98%

CXCR1 and CXCR2 enhances human melanoma tumourigenesis, growth and invasion

et al. 2009

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The aggressiveness of malignant melanoma is associated with differential expression of CXCL-8 and its receptors, CXCR1 and CXCR2. However, the precise functional role of these receptors in melanoma progression remains unclear. In this study, we investigate the precise functional role of CXCR1 and CXCR2 in melanoma progression. CXCR1 or CXCR2 were stably overexpressed in human melanoma cell lines, SBC-2 (non-tumourigenic) and A375P (low-tumourigenic) exhibiting low endogenous expression of receptors. Functional assays were performed to study the resulting changes in cell proliferation, motility and invasion, and in vivo tumour growth using a mouse xenograft model. Our data demonstrated that CXCR1-or CXCR2-overexpressing SBC-2 and A375P melanoma cells had enhanced proliferation, chemotaxis and invasiveness in vitro. Interestingly, CXCR1 or CXCR2 overexpression in SBC-2 cells induced tumourigenicity, and A375P cells significantly enhanced tumour growth as examined in vivo. Immunohistochemical analyses showed significantly increased tumour cell proliferation and microvessel density and reduced apoptosis in tumours generated from CXCR1-or CXCR2-overexpressing melanoma cells. CXCR1-or CXCR2-induced modulation of melanoma cell proliferation and migration was observed to be mediated through the activation of ERK1/2 phosphorylation.Together, these studies demonstrate that CXCR1 and CXCR2 play essential role in growth, survival, motility and invasion of human melanoma.

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IL-18 enhances SCF production of melanoma cells by regulating ROI and p38 MAPK activity

Cited by 22 publications

References 38 publications

Reversion of immune tolerance in advanced malignancy: modulation of myeloid-derived suppressor cell development by blockade of stem-cell factor function

CXCR1 and CXCR2 enhances human melanoma tumourigenesis, growth and invasion

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