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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A novel culture method has been developed to study the interaction of epithelial cells in the absence of a solid substratum. Starting with either a single cell suspension or aggregates, cells were floated at the interface of air and liquid culture medium. Two epithelial cell lines have been studied in this system: Madin-Darby canine kidney cells (MDCK), and a rat bladder tumor cell line (NBT-II). Starting with a single cell suspension of MDCK, the floating cells coalesced in 24 h into sheets of cells. The cells were morphologically polarized with the apical surface facing the liquid medium. Domes were observed regularly in these sheets of cells. NBT-II cells migrated actively from aggregates at the air-liquid interface. In this floating culture, NBT-II cells produced extensive cell processes similar to those seen in cells grown on a solid surface. Because cells at the air-liquid interface lack a solid substratum for adhesion, cell membrane processes such as lamellapodia, retraction fibers, pseudopods, and long, intercellular connections can only exert a tension equal to or less than the surface tension of the liquid. Dimethyl sulfoxide 2% stimulated desmosome formation in floating NBT-II cells, resulting in a cribriform pattern in the sheet of cells. This method of interface can lead to new understanding of morphogenesis of epithelial cells, and the mechanism of cell motility and formation of cell processess.
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PMID:Epithelial cell interaction in air-liquid interface culture. 273

Dipyridamole (DPD) has been shown to inhibit the motility of cells in culture. We have tested the effect of DPD on the invasion in confronting organ culture of the following malignant cell lines: mouse MO4 cells; rat NBT II bladder tumor cells; human SA4 glioblastoma cells; mouse LLC H61 lung carcinoma cells; and mouse F87 C1.6T2 melanoma x lymphocyte hybrid cells. At concentrations of 20 micrograms/ml or higher, DPD inhibited the invasion of all cell types into embryonic chick heart. In serum-free culture medium the anti-invasive concentration of DPD was about ten times lower. Anti-invasive concentrations of DPD also inhibited proliferation of the malignant cells. Both inhibition of invasion and of proliferation were reversible.
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PMID:Effect of dipyridamole on invasion of five types of malignant cells in organ culture. 277 69

Some neoplastic cell lines are readily killed when incubated in the presence of polyunsaturated fatty acids (PUFA). In an attempt to elucidate this phenomenon, we studied PUFA-driven superoxide (O2-) production by cultured NS-1 cells (murine lymphoid tumor cells). We find: (1) Even in the absence of added PUFA, NS-1 cells generate O2- (i.e., reduce nitroblue tetrazolium). (2) addition of PUFA increases O2- by greater than 50%. (3) Artificial loading of NS-1 cells with liposome encapsulated superoxide dismutase prevents the majority of spontaneous and PUFA-driven NBT reduction. We conclude that PUFA drives O2- generation by tumor cells, that this generation is largely intracellular, and that this phenomenon may help explain toxicity of PUFA for tumor cells.
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PMID:Polyunsaturated fatty acids stimulate superoxide formation in tumor cells: a mechanism for specific cytotoxicity and a model for tumor necrosis factor? 284 72

In an attempt to delineate the role of tumor-cell motility in the process of invasion, we compared the migration of NBT II in a two-dimensional migration assay with its migration in a three-dimensional invasion assay. Both systems were maintained with and without succinylated concanavalin A (s-Con A) dissolved in the culture medium. This lectin has a reversible inhibitory effect on the migration of cells in vitro. The migration of NBT-II aggregates, seeded in flasks containing 200 micrograms/ml s-Con A or without s-Con A, was studied by time-lapse photomicrography. In the presence of s-Con A, migration was immediately stopped. When the treated medium was replaced by culture medium to which 10 mM alpha-methyl-mannose was added, the inhibition of migration was abolished. The invasive capacity of NBT II in the presence or absence of s-Con A was studied by confronting precultured fragments of 9- to 11-day-old embryonic chick heart (0.4 mm in diameter) with NBT-II aggregates (0.2 mm) made in the presence or absence of s-Con A. Light microscopy showed no difference in the extent of invasion. To demonstrate the presence of s-Con A in the invading tumor cells, immunoperoxidase staining for Con A was done. The treated cultures stained positively while the controls were negative. The data presented here question the correlation between tumor-cell motility in two-dimensional system and the invasive behavior of these cells in three dimensions, and implies that the ability or inability of cells to migrate on plastic does not necessarily reflect their invasiveness in vitro.
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PMID:Migration inhibition of an epithelial cell line by s-Con A and the effect on its invasiveness. 286 26

Three human T-cell clones with activated killer activity (5B5, 5C1, and 7B5) which could lyse various tumor cell lines were established. The cytotoxic activity of these clones was decreased by incubation with anti-CD3 monoclonal antibody, suggesting that they recognized tumor cells by T-cell antigen receptor. A monoclonal antibody which blocked the cytotoxic activity of clone 5B5 was obtained. This antibody (N1977) blocked the binding and cytotoxic activity of clone 5B5 at the target cell level, suggesting that the antigen defined by N1977 antibody, designated as ATM-1, was a target molecule recognized by 5B5 cells. ATM-1 in the conditioned medium of a cancer cell line (NBT-2) and serum from a patient with lung cancer was characterized by following its immunoreactivity. On gel filtration, both the conditioned medium and the serum gave three peaks of ATM-1 immunoreactivity, corresponding to approximate molecular weights of 1,200,000, 700,000, and 120,000, respectively. They were chromatofocused at pH 4.0, 4.8, and 6.5, respectively. The high molecular weight forms were shown to be molecules with the disulfide-linked elementary glycoprotein with ATM-1 immunoreactivity and approximate molecular weight of 120,000. Most of the molecules with ATM-1 immunoreactivity bound to both concanavalin A and wheat germ agglutinin, and their binding activity to the antibodies was lost by treatment at 60 degrees C for 30 min. An assay of ATM-1 level in sera was performed by a sandwich enzyme immunoassay. The following positive percentages were obtained from preliminary clinical studies: breast cancer, 67% (8 of 12 cases); hepatocellular carcinoma, 83% (10 of 12 cases); gastric cancer, 58% (7 of 12 cases); lung cancer, 41% (5 of 12 cases); hematological malignancies, 0% (0 of 9 cases); systemic lupus erythematosus, 0% (0 of 8 cases); rheumatoid arthritis, 0% (0 of 8 cases).
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PMID:Identification of a tumor-associated target antigen, ATM-1, for a human T-cell clone with activated killer activity and its existence in sera of cancer patients. 304 79

The terminal differentiation, keratinization, of a rat bladder tumor cell line, NBT II, occurred in multicellular aggregates. After aggregation, these cells did not undergo a round of mitosis before keratinization. 5-Bromodeoxyuridine added to the monolayer cell culture 2 days before aggregation completely prevented this differentiation; it was ineffective when added at the time of cell aggregation. Vitamin A prevented the keratinization of NBT II cells in aggregates but did not inhibit aggregate formation; it enhanced the number of cells engaged in DNA synthesis. This model appears to be very useful for analyzing the mechanisms of terminal differentiation and its modulation by vitamin A in tumor cells.
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PMID:Keratinization and the effect of vitamin A in aggregates of a squamous carcinoma cell line NBT II. 615 20

To investigate the role played by developing microvessels in the spread of tumors, segments of rat aorta were cultured with aggregates of NBT-II-81, a cell line derived from squamous cell carcinoma of rat bladder. Aortic rings cultured in plasma clot gave rise to microvascular networks composed of branching endothelial channels. Aggregates of carcinoma in contract with fibrin clot alone grew slowly and by expansion. When the proliferating branching endothelial sprouts and channels contacted the tumor aggregates, the pattern of neoplastic growth changes abruptly, as carcinoma cells infiltrated the fibrin clot, migrating and proliferating in periendothelial location. Some vascular channels were disrupted and permeated by cords of invading tumor cells. Ultrastructural studies revealed intimate associated between invading epithelial cells and endothelial cells. Focal fusion of the endothelial basal lamina with the basal lamina of the tumor cells was observed. Our results demonstrate that angiogenesis in vitro, ie., in absence of active circulation, markedly enhanced the spread of a carcinoma in plasma clot and modified its pattern of growth. This indicates that other vascular-related factors beside nutritional gradients from the circulation attract tumor cells along endothelial paths.
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PMID:Angiogenesis-dependent tumor spread in reinforced fibrin clot culture. 618 44

Two epithelial cell lines of urological origin have been compared for their invasiveness in an in vitro three-dimensional culture system, using embryonic chick cardiac muscle as host tissue. Cells from the Nara bladder tumor line (NBT-II), an invasive tumor in the rat, invaded and progressively occupied the cardiac muscle which degenerated. Cells from a dog kidney line (MDCK), which are of low tumorigenicity in nude mice, failed to invade into the cardiac muscle in vitro. MDCK cells formed a structurally polarized epithelium around the heart tissue. MDCK is the first established epithelial cell line that has been found to grow in this invasion assay culture system and yet did not invade the heart fragment.
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PMID:Comparison of invasiveness and non-invasiveness of two epithelial cell lines in vitro. 648 Feb 88

The motility of an epithelial cell line NBT-II derived from a rat bladder tumor was examined on glass and on collagen. On glass the cells rotate in groups of 2-8 cells. Rotatory migration ceases as cells enter into mitosis; after mitosis, the daughter cells spread out and participate in the rotatory activity of the group. As the number of cells in a group increases the rate of rotatory migration slows, and groups with ten cells or more do not rotate consistently. On collagen NBT-II cells migrate as single cells in a smooth gliding fashion, with the broad lamellipodia as the leading front. After mitosis, the two daughter cells separate at 180 degrees of each other and migrate away independently. Before totally spreading out on the collagen surface, the pair of daughter cells shows a characteristic twist of about 60 degrees from their original position at telophase. The difference in motility of NBT II cells on glass and on collagen is explained in terms of differences in cell-to-cell cohesion and cell-to-substrate adhesion.
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PMID:Novel forms of epithelial cell motility on collagen and on glass surfaces. 715 Nov 40

Since one crucial step in tumor progression consists of the acquisition of invasive and metastatic properties, it is important to analyze the mechanisms used by cancer cells to disperse. Among the possible mechanisms of cell dispersion, cell motility appears as a central phenomenon that still needs to be understood at the molecular level. Our experimental approach to the contribution of cell motility in carcinoma cell dissemination is based on the study of the NBT-II rat bladder carcinoma cell line. The epithelial cell line gives rise to isolated, actively migrating, fibroblast-like cells in response to specific stimuli (collagens and acidic fibroblast growth factor [aFGF]). Analysis of the scattering response indicates that the different stimuli can synergize, leading to increased motility and invasiveness. NBT-II cells have two types of response to aFGF: they can either proliferate or scatter. In addition, the two responses are mutually exclusive, suggesting that the cell status can dictate whether or not tumor cells will disperse after exposure to a scatter factor. Finally, recent studies on the involvement of epithelial-specific cadherins in the process of aFGF-induced cell scattering indicate that a sustained expression of E-cadherin is not sufficient to protect cells from dispersing. In conclusion, our experimental model offers the opportunity to dissect the molecular events leading to tumor cell dissemination.
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PMID:Involvement of cell motility in tumor progression. 751 90


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