Interleukin-6 and the Network of Several Cytokines in Multiple Myeloma: An Overview of Clinical and Experimental Data

Lauta, Vito Michele

doi:10.1006/cyto.2001.0982

Cited by 77 publications

(54 citation statements)

References 59 publications

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“…TGFβ1 is present in the bone marrow (BM) environment and constitutes a pivotal molecule controlling BM cell proliferation and differentiation (27). Study in MM showed that IL-2 and IL-4 levels in patients were lower than those in the normal controls, whereas TGFβ1 level were higher than that in controls (3)(4)(5). TGFβ1 stimulates IL-6 transcripts in a time-and dosedependent manner in the in vitro study (28).…”

Section: Discussionmentioning

confidence: 99%

“…Several cytokines were reported to have pathological effect on the pathogenesis of the diseases. IL-6, TNF-α, IL-1 as well as transforming growth factor β1 (TGFβ1) were among these cytokines, which might be correlated with the disease severity, prognosis and predisposition (3)(4)(5). Biological studies supported a role for aberrant class switch recombination early in the natural history of the disease group suggesting that factors both in genetic and the environment may interact with this mechanism (6).…”

Section: Introductionmentioning

confidence: 99%

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Laboratory Characterizations on 2007 Cases of Monoclonal Gammopathies in East China

Wang

Gao

et al. 2008

Cell Mol Immunol

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Laboratory Characterizations on 2007 Cases of Monoclonal Gammopathies in East China

Wang

Gao

et al. 2008

Cell Mol Immunol

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“…Studies have pointed out IL-6 as an important osteoclast activating factor in different conditions with pathological osteoclastic bone resorption, e.g. arthritis and bone malignancies [4,21]. The importance of the RANIURANKL axis in bone metabolism has been elucidated and is undisputable.…”

Section: Discussionmentioning

confidence: 99%

Interleukin‐4 and interleukin‐13 potentiate interleukin‐1 induced secretion of interleukin‐6 in human osteoblast‐like cells

Silfverswärd

Frost

Brändström

et al. 2004

Journal Orthopaedic Research

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Formation of interleukin-6 (IL-6) in osteoblasts and bone marrow stromal cells is believed to regulate osteoclast recruitment. The anti-inflammatory cytokines interleukin-4 and -1 3 (IL-4 and IL-I 3) stimulate IL-6 production in human osteoblasts. We investigated the relative potencies, and synergistic effects, between IL-4, IL-13 and interleukin-1 (IL-1) on IL-6 formation in human osteoblast-like cells.Isolated human osteoblast-like cells were incubated for 72 h in the presence of various concentrations of IL-4, IL-13 and IL-1, and 1L-6 secretion was measured by ELISA. All cytokines stimulated the secretion of 1L-6. The rank order of potency was IL-1 >> 1L-4 > IL-13. There were no additive or synergistic effects between IL-4 and IL-13. However, co-stimulation with IL-I and IL-4 resulted in a marked synergistic effect on IL-6 secretion. Co-stimulation with IL-1 and IL-13 gave a minor synergistic effect. In conclusion, IL-4/13 synergistically potentiates IL-I induced secretion of IL-6 in human osteoblast-like cells.

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“…Interleukin-6 (IL-6) has been found in higher levels in wound fluids (Mateo et al, 1994;Gallo et al, 1997) and in tumors (Kawano et al, 1988;Meir et al, 1990;Okamoto et al, 1997). In multiple myelomas, IL-6 is known to be an autocrine growth factor and to protect them from apoptosis induced by various stimuli (Lauta, 2001). Evidence has been accumulating that IL-6 is an autocrine and paracrine growth factor for prostate cancer cell lines (Smith et al, 2001) and may contribute to the progression of prostate cancer (Chen et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Interleukin-6 acts as an antiapoptotic factor in human esophageal carcinoma cells through the activation of both STAT3 and mitogen-activated protein kinase pathways

Wong²,

et al. 2003

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The production of interleukin-6 (IL-6) has been discovered in a variety of human tumors. Here we report the expression of IL-6, IL-6 receptor a (IL-6Ra), and gp130 in human esophageal carcinoma tissues. We further demonstrate that IL-6 protects an esophageal carcinoma cell line CE48T/VGH from apoptosis induced by staurosporine. IL-6 stimulation induced a rapid phosphorylation of gp130 and STAT3, and a dominant-negative STAT3 completely abolished the antiapoptotic effect. IL-6 also activated ERK 1/2 in CE48T/VGH cells. Inhibition of the ERK activation by PD98059 and transfection of a dominant-negative ERK2 completely blocked the protection of IL-6 against apoptosis. Thus, both STAT and MAP kinase pathways are responsible for the IL-6-delivered survival signal in human esophageal carcinoma cells. In contrast, PI3-K inhibitors only partially attenuated the effect of IL-6, suggesting that PI3-K does not play a major role in the antiapoptotic signal of IL-6 in our system. To investigate whether IL-6 could induce the production of antiapoptotic molecules, proteins of the Bcl-2 family were measured. While Bcl-2, Bcl-x L, , and Bax were not affected, Mcl-1 was induced by IL-6 in human esophageal carcinoma cells. Our results suggest that IL-6 may contribute to the progression of esophageal cancers in an autocrine or paracrine manner.

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Interleukin-6 and the Network of Several Cytokines in Multiple Myeloma: An Overview of Clinical and Experimental Data

Cited by 77 publications

References 59 publications

Laboratory Characterizations on 2007 Cases of Monoclonal Gammopathies in East China

Laboratory Characterizations on 2007 Cases of Monoclonal Gammopathies in East China

Interleukin‐4 and interleukin‐13 potentiate interleukin‐1 induced secretion of interleukin‐6 in human osteoblast‐like cells

Interleukin-6 acts as an antiapoptotic factor in human esophageal carcinoma cells through the activation of both STAT3 and mitogen-activated protein kinase pathways

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