Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indole-3-acetic acid (IAA) activation by horseradish peroxidase (HRP) has been suggested as a new cancer therapy. Interestingly, we found that ultraviolet B UVB radiation also can activate IAA and produce free radicals in a dose-dependent manner. In this study, we attempted to identify the free radicals generated by UVB-irradiated IAA (IAAUVB), and to determine whether IAAUVB can induce the apoptosis of G361 human melanoma cells. Since IAA/HRP produces reactive oxygen species (ROS), we examined whether IAAUVB-generated radicals include ROS. Our results show that IAAUVB-induced free radical production is not inhibited by catalase, superoxide dismutase, or sodium formate, indicating that ROS are not generated by IAAUVB. On the other hand, IAAUVB caused lipid peroxidation, and this was blocked by Trolox, a water-soluble vitamin E derivative. Moreover, we found that IAAUVB caused apoptotic cell death and that this was inhibited by a low temperature. We further investigated IAAUVB-mediated apoptotic pathways, and found that IAAUVB causes caspase-8, Bid, caspase-3 activation, and poly (ADP-ribose) polymerase (PARP) cleavage. In addition, these apoptotic pathways were also blocked by low temperature. From these results, we propose that IAAUVB-induced free radicals cause human melanoma cell apoptosis via a death receptor-mediated apoptotic pathway.
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PMID:Light-activated indole-3-acetic acid induces apoptosis in g361 human melanoma cells. 1714 72

Although surgical removal is the most aggressive strategy to treat removable tumors, it sometimes aggravates tumor growth in metastatic sites. Because surgical procedures generate reactive oxygen species (ROS), known promoters of tumor metastasis and growth, we examined whether the growth of micrometastasis is inhibited by superoxide dismutase (SOD) derivatives after surgical removal of tumors in mice. Murine melanoma B16-BL6 cells were inoculated into the footpad to establish spontaneous pulmonary metastasis. The removal of the footpad tumor significantly (P < 0.05) increased the level of plasma lipoperoxides and the number of tumor cells in the lung. An intravenous injection of SOD or its pegylated-SOD derivative significantly (P < 0.05) inhibited the peroxidation and metastatic tumor growth. It also extended the survival period of mice undergoing removal of the footpad tumor. These findings indicate that the removal of tumor produces ROS, which then aggravates the growth of tumor cells in micrometastases. SOD derivatives can effectively prevent this metastatic tumor growth by detoxifying ROS.
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PMID:SOD derivatives prevent metastatic tumor growth aggravated by tumor removal. 1835 6

Polyhemoglobin is formed by the nanobiotechnological assembling of hemoglobin molecules into soluble nanodimension complex. A further step involves the nanobiotechnological assembly of hemoglobin, catalase and superoxide dismutase into a soluble nanodimension complex. This acts both as oxygen carrier and antioxidant to prevent the oxidative effects of hemoglobin. A further step is the preparation of nanodimension artificial red blood cells that contain hemoglobin and all the enzymes present in red blood cells. Other approaches include a polyhemoglobin-fibrinogen that acts as an oxygen carrier with platelet-like activity, and a polyhemoglobin-tyrosinase to retard the growth of a fatal skin cancer, melanoma.
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PMID:Nanobiotechnological modification of hemoglobin and enzymes from this laboratory. 1856 37

In humans both UV-A and UV-B can cause gene mutations and suppress immunity, which leads to skin cancer, including melanoma. Inhibition of reactive oxygen species (ROS) and reactive nitrogen species (RNS) appears particularly promising as ROS and RNS production by both UV-A and UV-B contributes to inflammation, immunosuppression, gene mutation and carcinogenesis. We evaluated the effect of two lichen compounds, sphaerophorin (depside) and pannarin (depsidone) on pBR322 DNA cleavage induced by hydroxyl radicals (()OH), and by nitric oxide (NO), and their superoxide anion (O(2)(-)) scavenging capacity. In addition, we investigated the growth inhibitory activity of these compounds against human melanoma cells (M14 cell line). Sphaerophorin and pannarin showed a protective effect on plasmid DNA and exhibited a superoxide dismutase like effect. The data obtained in cell culture show that these lichen metabolites inhibit the growth of melanoma cells, inducing an apoptotic cell death, demonstrated by the fragmentation of genomic DNA (COMET and TUNEL Assays) and by a significant increase of caspase-3 activity, and correlated, at least in part, to the increase of ROS generation, These results confirm the promising biological properties of sphaerophorin and pannarin and encourage further investigations on their molecular mechanisms.
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PMID:Lichen metabolites prevent UV light and nitric oxide-mediated plasmid DNA damage and induce apoptosis in human melanoma cells. 1872 17

Reactive oxygen species are implicated in cancer development and antioxidants in general and superoxide dismutases and superoxide dismutase mimetic in particular, and they inhibit malignant transformation. We examinated the effects of an isolated manganese superoxide dismutase from a medicinal plant Allium sativum. The protein was prepared by a serial of chromatographic techniques: gel filtration and diethylaminoethyl ions exchanger. The enzyme has a specific activity equal to 55 U/mg. Two tumoral cell lines, porcine endothelial cells and mouse melanoma cells were exposed to garlic superoxide dismutase. The exogenous manganese superoxide dismutase is able to modify the intracellular level of reactive oxygen species by eliminating superoxide anion and producing hydrogen peroxide. The cell viability of the two lines was not significantly affected but the cell multiplication was arrested. This effect obtained in the presence of manganese superoxide dismutase correlates with the activation and modulation of phospho-extracellular signal-regulated kinases proteins, implicated in the control of several biological processes including cell proliferation.
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PMID:Inhibitory effects of a manganese superoxide dismutase isolated from garlic (Allium sativum L.) on in vitro tumoral cell growth. 1920 37

There is now increasing evidence that free radicals and reactive oxygen species (ROS) are involved in a variety of pathological events. Reactive oxygen species are produced during normal cellular function and lead to lipid peroxidation, massive protein oxidation and degradation. Taurine is an abundant free amino acid in inflammatory cells, where it is thought to be cytoprotective. The aim of the present study was to examine whether taurine enhances endogenous antioxidant enzyme activity and/or regulates ROS generation in B16F10 mouse melanoma cells. B16F10 cells were exposed to medium containing taurine for a period of 24 h. Cell viability, measured by the MTT assay, exhibited a dose-dose dependent inhibition. Taurine increased the activities of superoxide dismutase, glutathione peroxidase and CAT compared to those of the control, an effect paralleling an increase in gene expression. Taurine also reduced ROS content in a dose-dependent manner. Taken together, our results suggest that taurine decreases ROS levels by increasing the levels of the antioxidant enzymes.
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PMID:Effect of taurine on antioxidant enzyme system in B16F10 melanoma cells. 1923 81

The 50% ethanolic extract (CH-ext) obtained from the unripe fruit of Citrus hassaku exhibited significant tyrosinase inhibitory activity. The CH-ext showed antioxidant activity, such as superoxide dismutase (SOD)-like activity and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical-scavenging activity. Activity-guided fractionation of the CH-ext indicated that flavanone glycoside-rich fractions showed potent tyrosinase inhibitory activity. Further examination revealed that the tyrosinase inhibitory activity and antioxidant activity of the CH-ext were attributable to naringin and neohesperidin, respectively. The CH-ext showed inhibition of melanogenesis without any effects on cell proliferation in cultured murine B16 melanoma cells after glucosamine exposure. The topical application of the CH-ext to the dorsal skin of brownish guinea pigs showed in vivo preventive effects against UVB-induced pigmentation.
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PMID:Inhibitory effects of Citrus hassaku extract and its flavanone glycosides on melanogenesis. 1925 87

Histamine is a recognized growth factor in melanoma, and exogenous histamine produces a dual effect on proliferation. We have previously reported that histamine at micromolar concentrations reduces the proliferation of melanoma cell lines. To investigate the mechanism by which histamine inhibits proliferation of WM35 human melanoma cells, we have studied the involvement of histamine in reactive oxygen species production and antioxidant enzyme regulation in these cells. Results indicate that histamine treatment (10 microM) significantly increased hydrogen peroxide levels, whereas it slightly decreased superoxide levels associated with an enhancement of superoxide dismutase and a reduction in catalase activity. Additionally, catalase treatment reversed the inhibitory effect of histamine on proliferation, and various treatments that reduce hydrogen peroxide formation increased proliferation of these cells. Furthermore, we demonstrate that the inhibition of proliferation produced by histamine was mediated at least in part by an induction of cell senescence. We conclude that hydrogen peroxide is involved in histamine-mediated modulation of proliferation in malignant melanoma cells.
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PMID:Involvement of hydrogen peroxide in histamine-induced modulation of WM35 human malignant melanoma cell proliferation. 1928 50

Constitutive ERK activation, superoxide dismutases (SOD) and p53 mutations are implicated in modulating tumor apoptotic response. We now investigated whether human melanoma survival in response to sodium nitroprusside (SNP) is modulated by: (a) stable introduction of a DN-mutant p53; (b) pharmacologically inhibiting ERK activation with UO126; (c) addition of exogenous SOD. Nitroprusside releases nitric oxide (NO) when intact, or acts in a NO-independent manner via iron and residual cyanide after light exposure (lex-SNP). When tested at 300 microM in 72 h treatments by cytometric live-dead assays, intact SNP caused a 50% lethality versus a 30% lethality induced by lex-SNP. No protection from SNP toxicity was seen when inhibiting the PI3-kinase pathway with LY294002 or c-Jun NH(2) kinase signaling with SP600125. However, pretreatment with UO126 protected from SNP-mediated cell death including counteracting apoptosis-associated Bax expression and PARP cleavage, plus reversing loss of Cu,Zn-SOD. Moreover, addition of exogenous SOD also protected cells from SNP toxicity. In spite of the greater earlier effects of intact SNP, cells treated with single doses of either intact or lex-SNP, revealed about a 90% mortality in longer 120 h treatments, and these were also counteracted by UO126 or exogenous SOD. This report is the first to show that: constitutive ERK activation characteristic of cancer cells, increases a nitroprusside-induced apoptosis modulated by SOD.
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PMID:ERK activation increases nitroprusside induced apoptosis in human melanoma cells irrespective of p53 status: role of superoxide dismutases. 1939 58

In a previous study, we demonstrated that baicalein induces hydroxyl radical formation in human platelets but the mechanisms are unclear. Herein, we show, using an electron spin resonance technique, that baicalein also induces hydroxyl radical formation in B16F10 melanoma cells in a dose-dependent manner. Baicalein produced superoxide anions in the presence of an iron chelator and superoxide dismutase (SOD) inhibitor. We suggest that superoxide anions produced by baicalein were promptly converted to hydroxyl radicals through SOD and the Fenton reaction in B16F10 melanoma cells. According to Western blotting results, the 12-LOX protein was expressed in B16F10 melanoma cells, but baicalein had no effect on 12-LOX expression. Decreases in 12-LOX protein expression and hydroxyl radical signals occurred in a 12-LOX small interfering RNA knockdown protein group compared with the baicalein control. In the MTT assay, we also found that baicalein caused a reduction in cellular viability, which was reversed by the addition of ROS scavengers. On the basis of these data, we conclude that ROS formation catalyzed by 12-LOX is one possible mechanism of growth inhibition by baicalein in B16F10 melanoma cells.
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PMID:Baicalein induces proliferation inhibition in B16F10 melanoma cells by generating reactive oxygen species via 12-lipoxygenase. 1943 16


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