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)

The alkyllysophospholipid analog 1-0-octadecyl-2-0-methyl-3-phosphorylcholine (ET-18-OCH3) was examined for possible anti attachment effects on B16-F10 murine melanoma cells in vitro. At sub-lethal lipid concentrations B16-F10 cells were inhibited from attaching to reconstituted basement membrane (Matrigel) during a 45 min assay. This type of inhibition was also imparted by the isoprenoid farnesol but not by egg lysophosphatidylcholine (LPC) at concentrations up to 10 micrograms/ml. Both lipids were toxic to B16-F10 cells in the absence of bovine serum albumin (BSA), BSA (0.1%) completely protected the cells from lysis except when both lipids were combined as a mixture. Light and electron microscopy, as well as electronic sizing of cells, gave evidence of alkyllysophospholipid induced reduction in cell size which correlated well with attachment inhibition. The results suggest that alkyllysophospholipid induced reduction of cell surface area leads to inhibition of cell attachment to basement membrane which 8 with our experimental conditions, was not permanent since cells eventually attach within 24 h after treatment. The enhanced lytic effect the lysophospholipid imparts on the alkyl compound, in conjunction with the anti-attachment properties should be important areas for future research.
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PMID:Alkyllysophospholipid influenced melanoma cell morphology is associated with decreased attachment to basement membrane. 144 Sep 71

The antifungal reagent Fungizone (amphotericin B and deoxycholate) caused an activation in dopachrome tautomerase and dopa oxidase activities of B16/F10 melanoma cells at the routine concentration (2.5 micrograms/ml) used for preventing molds and yeast growth in cultures of animal cells. However, higher amphotericin B concentrations caused a significant cell death and the inhibition of enzymatic activities. At the optimal concentration of Fungizone, the enzymatic activities and melanin content were augmented as incubation time increased. The detergent sodium deoxycholate alone exerted no effect on these melanogenic parameters, eliminating the possibility that this detergent was partially responsible for melanogenic modifications produced by Fungizone. After withdrawal of Fungizone from the reaction medium, the recovery of melanogenic parameters to normal values was slower for DCT than for tyrosinase. The behavior of dopa oxidase was very similar to that reported by Johnson and Bagnara (Pigment Cell Res. 3, 173-175) for tyrosine hydroxylase.
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PMID:Effect of amphotericin B on dopachrome tautomerase activity and other melanogenic parameters in cultured B16/F10 melanoma cells. 149 75

(-)-Epigallocatechin gallate (EGCG), the main polyphenolic constituent of green tea, inhibits tumor promotion and chemical carcinogenesis in animal experimental systems. Here we report that the peroral administration of EGCG inhibited metastasis of B16 melanoma cell lines, such as B16-F10 and BL6, in both experimental and spontaneous systems.
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PMID:Effect of (-)-epigallocatechin gallate, the main constituent of green tea, on lung metastasis with mouse B16 melanoma cell lines. 151 9

Initial adhesion of B16 melanoma variants to non-activated endothelial cells is mediated through specific interaction between GM3 (NeuAc alpha 2----3Gal beta 1----4Glc beta 1----Cer) expressed on melanoma cells and lactosylceramide (LacCer, Gal beta 1----4Glc beta 1----Cer) expressed on endothelial cells. This adhesion is predominant over integrin- or lectin-mediated adhesion in a dynamic flow experimental system employing a parallel plate laminar flow chamber (Lawrence, M. B., Smith, C. W., Eskin, S. G., and McIntire, L. V. (1990) Blood 75, 227-237). In this system, a tumor cell suspension flows over a glass plate coated with glycosphingolipid, lectin, or fibronectin, and adhesion is recorded on videotape. These conditions were designed to mimic the microvascular environment in which tumor metastatic deposition takes place. In contrast, lectin- and fibronectin-based mechanisms are predominant in previously used static adhesion systems. Under static conditions, the relative degree of adhesion of the four B16 variants to endothelial cells or to LacCer-coated plates was the same as their relative degree of GM3 expression (i.e. BL6 approximately F10 greater than F1 greater than WA4), and adhesion was inhibited in the presence of methyl-beta-lactoside, or liposomes containing LacCer or GM3. Adhesion was also inhibited by pretreatment of B16 cells with anti-GM3 antibody DH2 or sialidase and by pretreatment of endothelial cells with anti-LacCer antibody T5A7. Under dynamic flow conditions, WA4 cells did not adhere to mouse endothelial cells at high shear stress (greater than 2.5 dynes/cm2) but did adhere at lower shear stress. In contrast, BL6 and F10 cells adhered strongly at both low and high shear stress. BL6 cell adhesion to endothelial cells at both low and high shear stress was inhibited in the presence of antibody DH2, ethyl-beta-lactoside, or lactose, as well as by pretreatment of BL6 cells with sialidase. Thus, some clear differences, as well as similarities, in cell adhesion under static versus dynamic conditions are demonstrated. These findings suggest that melanoma cell adhesion to endothelial cells, based on GM3/LacCer interaction, initiates metastatic deposition, which may trigger a series of "cascade" reactions leading to activation of endothelial cells and expression of Ig family or selectin receptors, thereby promoting adhesion and migration of tumor cells.
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PMID:Cell adhesion in a dynamic flow system as compared to static system. Glycosphingolipid-glycosphingolipid interaction in the dynamic system predominates over lectin- or integrin-based mechanisms in adhesion of B16 melanoma cells to non-activated endothelial cells. 151 64

The cytolytic and/or cytostatic effects of hyperthermia, lymphokine-activated killer cells (LAK cells) and the combination of both were assayed using F1 and F10 B16 melanoma cell lines. F10 cells with a high metastatic potential showed a greater sensitivity to hyperthermia than F1 cells which have low metastatic potential. The F10 cells were lysed to a lesser extent by LAK cells than the F1-B16 cells. When the cell lines were subjected to hyperthermia at 43 degrees C for 3 h and then interacted with LAK cells, the maximum cytolysis reached almost 100%. When the interaction with LAK cells was followed by hyperthermia at 43 degrees C, the total release of 51Cr from the cell lines was 75-85%. The extent of 51Cr release from the B16 melanoma cell lines was inversely correlated with the survival rate as calculated by the plating efficiency of the incubated cells. The survival rate of mice intravenously injected with B16-F10 cells and subjected to hyperthermia at 41 degrees C for 3 h in vitro increased compared to that of controls. This was further increased by the simultaneous administration of LAK cells.
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PMID:Responses of B16 melanoma cell lines, F1 and F10, to hyperthermia, lymphokine-activated killer cells and a combination of both in vitro. 153 78

The 90-kD lung endothelial cell adhesion molecule-1 (Lu-ECAM-1) selectively promotes Ca(2+)-dependent adhesion of lung-metastatic B16 melanoma cells. Corresponding with their metastatic performance, high lung-metastatic B16-F10 melanoma cells bind in significantly higher numbers to Lu-ECAM-1 than their intermediate and low lung-metastatic counterparts B16-L8-F10 and B16-F0, respectively. Maximum attachment is observed at a density of approximately 2.4 x 10(2) Lu-ECAM-1 sites/microns2 of plastic surface. B16 melanoma cell binding to Lu-ECAM-1 is blocked by mAb 6D3 and is competitively inhibited by soluble Lu-ECAM-1. C57B1/6 mice passively immunized with anti-Lu-ECAM-1 mAb 6D3 or actively immunized with purified Lu-ECAM-1 exhibit an anti-Lu-ECAM-1 antibody titer-dependent reduction in the number of B16 experimental metastases. Lu-ECAM-1 promotes neither binding nor metastasis of other lung-metastatic tumor cells (e.g., KLN205). Our data indicate that an "antiadhesion" therapy directed at interfering with the adherence of blood-borne tumor cells to organ-specific vascular endothelium is efficient in the control of metastasis formation in selective organ sites.
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PMID:Blocking of lung endothelial cell adhesion molecule-1 (Lu-ECAM-1) inhibits murine melanoma lung metastasis. 160 82

Bufalin, which is one of prominent components of Chinese toad venom, was found to decrease the rate of cell proliferation of mouse melanoma clone B16-F10 cells and a concomitant stimulation of expression of its melanotic phenotype. The effect of bufalin on melanogenesis included stimulation of tyrosinase activity and increase of cellular melanin content. These effects became apparent after 48 hr exposure to 10(-4) M bufalin and increased thereafter. Other cardiotonic steroids, such as cinobufagin and ouabain, at the concentration of 10(-4) M for 6 days, also showed the stimulatory effect on melanin synthesis of B16-F10 cells, but not digitoxigenin.
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PMID:Stimulation of melanin synthesis of B16-F10 mouse melanoma cells by bufalin. 161 70

The chorioallantoic membrane of chick embryos was used to examine the responses of three tumour cell lines to anticancer agents, alone and in combination with hyperthermia. Fifteen minutes of hyperthermia at 42.5 degrees C produced the most favourable anticancer effect in the B16-F10 grafts. The use of Adriamycin (ADM) alone and the combined use of hyperthermia and either cisplatin (CDDP), cyclophosphamide (CY) or ADM resulted in a significantly higher rate of tumour regression in the B16-F10 grafts from a murine melanoma. In the KK-47 grafts derived from a transitional cell carcinoma of the bladder, the use of CY alone and the combination of CY and hyperthermia produced a significant tumour regression rate. In the T24 grafts neither the use of CY or CDDP alone, nor the combination of these drugs with hyperthermia demonstrated any significant effect. This method of screening anticancer agents was found to be rapid, simple to perform and inexpensive.
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PMID:Responses of tumour cell lines implanted onto the chorioallantoic membrane of chick embryo to anticancer agents in combination with hyperthermia. 161 86

In vivo experiments performed with NIH (nu/nu, bg/bg, xid/xid) triple immunodeficient (TD) mice revealed the striking ability of i.v. injected B16-F1 and B16-F10 murine melanoma cells to colonize not only the lungs but also the liver of TD mice. Subsequently, B16 melanoma cell cultures, which express very low levels of H-2Kb antigen, were cotransfected with plasmids pRSVneo, containing the neomycin resistance gene, and 6-2B1pMT, expressing the H-2Kb complentary DNA under the control of the metallothionein enhancer-promoter. Several neomycin-resistant clones were analyzed for H-2Kb and H-2Db expression by RNase protection and flow cytometry assays. All parental lines and transfected clones expressed normal levels of H-2Db mRNA, while only some of the transfected clones expressed easily detectable levels of H-2Kb mRNA. Moreover, in these clones H-2Kb expression could be enhanced in the presence of Zn2+, indicating that the metallothionein enhancer was functioning properly. Parental cells and transfected clones were injected i.v. in TD mice to assess the possible involvement of H-2Kb antigen in regulating the metastatic potential of B16 melanoma cells. We observed a remarkable correlation between expression of H-2Kb antigen and suppression of liver-specific metastases in TD mice. Identical results were obtained when we gave TD mice injections of mixed populations of transfectants expressing H-2Kb antigen, obtained by fluorescence-activated cell sorting. These experiments allowed us to rule out the possibility that the observed changes in metastatic potential were due to clonal variability among individual transfected clones. Taken together, the results of our in vivo studies with immunodeficient mice support the notion that specific major histocompatibility complex Class I molecules modulate the metastatic potential of malignant cells also by mechanisms which are independent of their well-established role in antigen presentation.
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PMID:Expression of a transfected H-2Kb gene in B16 cells correlates with suppression of liver metastases in triple immunodeficient mice. 161 80

N-linked oligosaccharide moieties of cell surface glycoconjugates may be involved in the metastatic potential of tumour cells. Many studies have examined the anti-metastatic properties of inhibitors of carbohydrate synthesis or processing in vitro. However, there has so far been little evidence of such inhibitory factors on metastasis in vivo because of the general high toxicity of the inhibitors. In this study, we found nojirimycin (NM) to be a substantially non-toxic carbohydrate synthesis inhibitor that inhibited the experimental metastasis of B16-F10 melanoma cells not only in vitro but also in vivo. When NM was administered intraperitoneally to syngeneic C57BL/6 mice, the inhibition was dose-dependent, with 40-75% suppression of pulmonary colonization observed after 5 days exposure to NM (at 0.4 or 4 mg/day). An in vitro lectin sensitivity assay showed that NM-treated B16-F10 cells were less susceptible to the lectin concanavalin-A, suggesting alteration or decrease of high mannose-type carbohydrate moieties on the cell surface. Further in vitro analysis of adhesiveness between B16-F10 cells and endothelial cells demonstrated that NM treatment causes reduced binding of B16-F10 cells to endothelial cells. We have also studied the effect of NM on natural killer (NK) cells in mice. NM treatment elicited no substantial increase in the cytotoxic activity of splenic NK cells against YAC-1 target cells. These results indicate that NM acts on the process of adhesion and that specific structures of the cell surface carbohydrate moieties may be involved in the colonization phase of metastasis in vivo.
Melanoma Res 1992 May
PMID:Role of asparagine-linked carbohydrates in pulmonary metastasis of B16-F10 murine melanoma cells: implication through glycosylation inhibition by nojirimycin. 164 22


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