Autocrine interleukin-1 receptor antagonist can support malignant growth of glioblastoma by blocking growth-inhibiting autocrine loop of interleukin-1

Oelmann, Elisabeth; Kraemer, Annette; Serve, Hubert; Reufi, B; Oberberg, D; Patt, Stephan; Herbst, Hermann; Stein, Harald; Thiel, Eckhard; Berdel, Wolfgang E.

doi:10.1002/(sici)1097-0215(19970611)71:6<1066::aid-ijc25>3.0.co;2-a

Cited by 48 publications

(29 citation statements)

References 61 publications

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“…Many cancers are known to arise from sites with inflammation (Mantovani et al, 2008). In addition, IL-1b is also detected in various tumor types (Culig et al, 1998;Jin et al, 1997;Oelmann et al, 1997;Saijo et al, 2002), where its expression is associated with tumor invasiveness and angiogenesis (Carmi et al, 2009;Voronov et al, 2003), suggesting a possible role for the inflammasome in tumorgenesis. In line with this, late stage human melanoma cells were demonstrated to spontaneously secrete active IL-1b via constitutive activation of the NLRP3 inflammasome in the absence of exogenous stimulation, exhibiting a feature of autoinflammatory diseases (Okamoto et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Inflammasome polymorphisms confer susceptibility to sporadic malignant melanoma

Verma

Bivik

Farahani

et al. 2012

Pigment Cell Melanoma Res

106

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SummaryGenetic variants of NLRP3 and NLRP1 are known to modulate levels of pro‐inflammatory cytokine interleukin (IL)‐1β. The purpose of this study was to investigate the association of NLRP3/NLRP1 polymorphisms with susceptibility and clinical features of malignant melanoma in a Swedish case–control study. Common variants in NLRP3/NLRP1 were investigated in sporadic malignant melanoma patients and healthy controls followed by analysis using logistic regression. NLRP3 variant (rs35829419) was significantly more common in male patients than in controls (OR, 2.22; CI, 1.27–3.86). Upon stratification, significant association with nodular melanoma was observed (OR, 2.89; CI, 1.33–6.30), which intensified in male patients (OR 4.03, CI 1.40–11.59). The NLRP1 variant (rs12150220) was significantly more common in fair‐skinned female patients (OR, 1.85; CI, 1.04–3.33) and showed strong associations with nodular melanoma (OR, 6.03; CI, 1.33–25). Our data suggest that NLRP3/NLRP1 polymorphisms are associated with melanoma susceptibility; these findings warrant validation in other independent populations.

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Section: Discussionmentioning

confidence: 99%

Inflammasome polymorphisms confer susceptibility to sporadic malignant melanoma

Verma

Bivik

Farahani

et al. 2012

Pigment Cell Melanoma Res

106

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“…Many authors have recently reported that endogenous IL-1/IL1ra balance regulates the homeostasis of cell proliferation and cell death (Corradi et al, 1995;Furukawa et al, 1995;Goletti et al, 1996;Oelmann et al, 1997). In various types of cells, the production and secretion of IL-1 and IL-1ra is simultaneous.…”

Section: Discussionmentioning

confidence: 99%

“…Friedlander et al (1996) reported that the ICE downregulates IL-1β-IL-1 receptor-binding activity, which causes the resistance to IL-1β. Furthermore, many authors have recently reported that endogenous IL-1 and IL-1ra balance regulates cell proliferation in many cell types (Corradi et al, 1995;Furukawa et Overexpression of IL-1ra gene up-regulates interleukin-1β converting enzyme (ICE) gene expression: possible mechanism underlying IL-1β-resistance of cancer cells Oelmann et al, 1997), although it remains unclear how this balance can be regulated in these cells. Thus, both IL-1ra and ICE seem to be closely associated with IL-1-mediated cell proliferation and/or cell death.…”

mentioning

confidence: 99%

Overexpression of IL-1ra gene up-regulates interleukin-1β converting enzyme (ICE) gene expression: Possible mechanism underlying IL-1β-resistance of cancer cells

et al. 1999

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Ala-Asp-CHO (YVAD-CHO) blocked IL-1β-induced growth inhibition in KU-1 and KU-2. Overexpression of the secretory type IL-1ra with adenovirus vector (AxIL-1ra) enhanced ICE gene expression, while exogenous IL-1ra (100 ng ml -1 ) did not enhance it. Furthermore, AxIL-1ra treatment promoted endogenous IL-1β secretion and induced significant growth inhibition and apoptotic cell death on . Treatment with either IL-1ra (100 ng ml -1 ), IL-1β antibody (100 µg ml -1 ), or YVAD-CHO blocked AxIL-1ra-induced cell death in . These results suggest that IL-1β-sensitivity depends on the level of ICE gene expression, which is regulated by the level of endogenous sIL-1ra expression. This is a first report on the intracellular function of sIL-1ra and these findings may provide key insights into the mechanism underlying the viability of cancer cells.

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“…Oelmann and cols, performed a study in cell lines of glioblastoma showed that IL1Ra modulates glioblastoma growth. Experimental addition of neutralizing antibody against IL1Ra down-regulated growth of IL1 and IL1Ra producing glioblastoma, the authors suggest that an autocrine production of IL1Ra can counteract IL1 function and represent a basic escape mechanism malignant growth in some glioblastomas (Oelmann et al, 1997).…”

Section: Oncogenesismentioning

confidence: 99%

“…IL1RN is expressed physiologically in different tissues like lymph node, brain, heart, colon, adipocyte, kidney, liver, lung, thyroid, adrenal gland, skin, placenta, ovary, prostate and testis (GeneCards). Furthermore, IL1RN is present in numerous cancers such as gastric cancer (Iizuka et al, 1999), cervical cancer (Fujiwaki et al, 2003), lymphoblastic (Hulkkonen et al, 2000) and myelogenous (Estrov et al, 1992) leukemias, breast cancer (Miller et al, 2000), endometrial cancer , bladder cancer (Ahirwar et al, 2009), colorectal cancer (Viet et al, 2005), lung cancer (Lind et al, 2005) and brain tumors (Oelmann et al, 1997;Ilyin et al, 1998).…”

Section: Expressionmentioning

confidence: 99%