Interleukin-1-induced Growth Inhibition of Human Melanoma Cells

Yang, De; Hayashi, Hidetoshi; Takii, Takemasa; Mizutani, Yukiko; Inukai, Yoshitaka; Onozaki, Kikuo

doi:10.1074/jbc.272.6.3376

Cited by 31 publications

(10 citation statements)

References 57 publications

(50 reference statements)

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“…It should be noted that IL-1 reportedly induces antizyme expression, which is responsible for IL-1-induced growth inhibition of human melanoma cells through downregulation of ODC activity (Yang et al, 1997). These previous studies suggest that ectopic antizyme expression may counteract the eect of ODC upregulation and lead to anti-tumor activity.…”

Section: Discussionmentioning

confidence: 99%

Anti-tumor activity of antizyme which targets the ornithine decarboxylase (ODC) required for cell growth and transformation

et al. 1999

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Cell proliferation and transformation induced by growth factor stimulation or by carcinogens, viruses, or oncogenes are characterized by an associated increase in polyamine levels, which is mediated by increased polyamine biosynthesis and enhanced uptake of polyamines. Polyamine biosynthesis is catalyzed particularly, in the level of ornithine decarboxylase (ODC). The elevation of cellular polyamine levels on the other hand accelerates the induction of ornithine decarboxylase antizyme (antizyme), which is involved not only in ODC-degradation, but in the negative regulation of polyamine transport. Taking advantage of these characteristics of antizyme, the potential of antizyme as a factor having anti-cell growth and anti-tumor activity was investigated. We show that antizyme can induce cell death associated with a rapid decline of intracellular polyamine contents. The possible anti-tumor activities of ectopically expressed antizyme were tested in p21H-ras (Val 12)-transformed NIH3T3 cells and several human malignant cell lines including a line with loss of p53 expression, and they were shown to be as sensitive as nontransformed NIH3T3 cells in vitro. The in vivo antitumor activity was also tested using nude mice inoculated with H-ras transformed NIH3T3 cells that had been transfected with inducible antizyme expression vector and the results showed that antizyme expression in vivo blocks tumor formation in these mice. These results suggest that ectopic antizyme expression is of possible therapeutic bene®t in the treatment of cancer, which is mediated by ODC inactivation and intracellular polyamine depletion.

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Section: Discussionmentioning

confidence: 99%

Anti-tumor activity of antizyme which targets the ornithine decarboxylase (ODC) required for cell growth and transformation

et al. 1999

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“…For instance, in human thymocytes, B cells and fibroblasts, IL-1β acts as a growth stimulator for the cell proliferation (3-5), while growth of some other cells, such as human endothelial cells, breast carcinoma cells, mouse myeloid leukemia cells and human melanoma cells, is inhibited by IL-1β (6-9). Previous studies reported that IL-1β induced growth inhibition in human melanoma cells through down-regulation of ornithine decarboxylase (ODC) (10, 11), up-regulation of IL-6 (12) and cell cycle arrest (13). Research carried out by Itoh and his coworkers also indicated that this antiproliferative effect was mediated by p38 mitogen-activated protein kinase (p38 MAPK) (14).…”

Section: Introductionmentioning

confidence: 99%

IL-1β Acts in Synergy with Endogenous IL-1β in A375-S2 Human Melanoma Cell Apoptosis Through Mitochondrial Pathway

et al. 2005

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Interleukin-1β (IL-1β) is a pivotal proinflammatory cytokine. To investigate the mechanism of IL-1β-induced cell death in human malignant melanoma A375-S2 cells, MTT assay, photomicroscopical observation, DNA agarose gel electrophoresis, radioimmunoassay and Western blot analysis were carried out. IL-1β did not only induce nuclear condensation and DNA fragmentation, but also increased degradation of two substrates of caspase-3, poly ADP-ribose polymerase (PARP) and inhibitor of caspase-activated DNase (ICAD). Simultaneously, release of precursor of IL-1β (pro-IL-1β) and endogenous IL-1β production were involved in the apoptotic process. IL-1β enhanced the ratio of Bax/Bcl-2 and Bax/Bcl-xL expression and up-regulated apoptosis inducing factor (AIF) expression, which required the activation of downstream caspases. These results suggest that IL-1β induces endogenous IL-1β production, enhances cleavage of caspase downstream substrates and promotes mitochondria mediated apoptosis in A375-S2 cells.

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“…11) Previous studies reported that IL-1 induced growth inhibition in human melanoma cells through down-regulation of ornithine decarboxylase (ODC), 16,17) up-regulation of IL-6 18) and cell cycle arrest. 19) Research carried out by Itoh and his coworkers also indicated that this antiproliferative effect was mediated by p38 MAPK.…”

Section: )mentioning

confidence: 99%

Evodiamine Induced Human Melanoma A375-S2 Cell Death Partially through Interleukin 1 Mediated Pathway

Che

Wang

Tashiro

et al. 2005

Biological & Pharmaceutical Bulletin

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Evodiamine, a constituent isolated from the dried, unripe fruit of Evodia rutaecarpa BENTHAM (go-shu-yu in Japanese) has been reported to present bronchial contractive, 1) catecholamine secretory, 2) vasodilatory, 3,4) anti-nociceptive 5) and antitumor effect.6) It was also reported that evodiamine had an inhibitory effect on tumor cell migration in vitro.7) Our previous study showed that up-regulation of Bax/Bcl-2 amplified the activation of caspase cascade, resulting in apoptosis in A375-S2 cells. Additionally, simultaneous activation of p38 mitogen-activated protein kinase (MAPK) and inhibition of extracellular signal-regulated protein kinase (ERK) activity contributed to evodiamine-induced necrosis at later stage. 8)Interleukin 1 (IL-1) is one of the multifunctional cytokines produced predominantly by activated monocytes and macrophages.9) Among the IL-1 family, IL-1a and IL-1b are referred to be "agonist" molecules that exert not only pleiotropic effects in host reactions such as immune defence, inflammation and homeostasis, 10,11) but also regulates a variety of cell functions of many cell types in both positive and negative manners.12-15) However, the third member IL-1 receptor antagonist (IL-1Ra) binds to the same receptors as IL1a or b, but does not induce any intracellular signal, therefore, acts as a natural inhibitor of IL-1.11) Previous studies reported that IL-1 induced growth inhibition in human melanoma cells through down-regulation of ornithine decarboxylase (ODC), 16,17) up-regulation of IL-6 18) and cell cycle arrest. 19) Research carried out by Itoh and his coworkers also indicated that this antiproliferative effect was mediated by p38 MAPK. 20) Our study has further confirmed that induction of Fas-ligand (Fas-L), activation of caspases, regulation of Bcl-2 family proteins and induction of endogenous IL-1b also contributed to IL-1b-induced A375-S2 cell death (data not shown). Therefore, there seem to be some similarities between evdiamine's and IL-1's anti-tumor machinery.Engagement of the extracellular domain of Fas by the Fas-L results in intracellular recruitment of caspase-8 to Fas via the adaptor protein, Fas-associated death domain (FADD) protein, because FADD interacts with Fas through its death domain and with caspase-8 through a death effector domain.21) Activation of caspase cascade was responsible for the consequent process that couples DNA damage and p53 activation to pro-or anti-apoptotic machinery involves in the Bcl-2 family proteins.8,22) Bcl-2 family was known to play essential roles in DNA damage-induced apoptosis. 23,24) In addition, p53 induction increases pro-apoptotic Bax synthesis 25) and activates Ras/Raf/MAPK cascade. 26)In the present study, we demonstrated that evodiamine induced A375-S2 melanoma cell death partially through IL-1 mediated pathway. Human melanoma is the most aggressive form of skin cancer and is becoming resistant to all current modalities of cancer therapy. The major aim of our study is to find out new target of natural product and develop specific ...

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Interleukin-1-induced Growth Inhibition of Human Melanoma Cells

Cited by 31 publications

References 57 publications

Anti-tumor activity of antizyme which targets the ornithine decarboxylase (ODC) required for cell growth and transformation

Anti-tumor activity of antizyme which targets the ornithine decarboxylase (ODC) required for cell growth and transformation

IL-1β Acts in Synergy with Endogenous IL-1β in A375-S2 Human Melanoma Cell Apoptosis Through Mitochondrial Pathway

Evodiamine Induced Human Melanoma A375-S2 Cell Death Partially through Interleukin 1 Mediated Pathway

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