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Results for “Cell metastasis”

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At least 19 recordsLinked to original sources
PubMed2025

Glutamate molecular structure and protein affect the inhibition of breast cancer cell metastasis: Cell-derived exosomes inhibitory effects through the MAPK signaling pathway.

The aim of this study was to investigate the inhibitory effect of glutamate molecular structure and protein on breast cancer cell metastasis and the potential inhibitory mechanism of cell-derived exosomes via MAPK signaling pathway. Breast cancer cell lines with high metastatic potential were selected by in vitro cell culture technique. The effects of specific inhibitors of glutamic acid on the proliferation and metastasis of breast cancer cells were studied. Changes in protein expression profiles were analyzed by proteomics techniques to identify key proteins associated with breast cancer metastasis. Breast cancer cells were treated with inhibitors of the MAPK signaling pathway to evaluate their effect on cell metastasis and compare with exosome treatment. The results showed that the specific inhibitors of glutamate molecular structure could significantly inhibit the proliferation and metastasis of breast cancer cells. Proteomic analysis revealed several down-regulated proteins that are closely related to breast cancer metastasis.

Humans↗
PubMed1987

Thrombospondin, a potentiator of tumor cell metastasis.

The platelet-secreted protein thrombospondin (TSP) potentiates tumor cell metastasis. Human TSP injected i.v. into mice 5 min prior to i.v. injection of T241 sarcoma cells potentiates lung tumor colony formation. Several lines of evidence suggest that the TSP-enhancing effect involves both TSP-mediated tumor cell adhesion and the host's hemostatic system: TSP potentiates the initial, rapid sequestering of tumor cells in the lung; TSP promotes the adhesion of tumor cells in vitro; the effect of TSP on tumor cell metastasis is dependent on the presence of platelets and a normal plasma clotting system, since TSP does not potentiate lung tumor colony formation in either thrombocytopenic mice or mice anticoagulated with Coumadin. Our results suggest a central role for TSP in the metastatic process.

Animals↗
PubMed1989

The combined effect of interferon and 5-FU on tumor-cell metastasis in the nude mouse.

In searching for a suitable animal model system to study colorectal tumor-cell metastasis, the method of injecting tumor cells directly into the spleen of athymic nude mice was explored. The cells used in this study consisted of the Colo 205 cell line, isolated and established from the ascitic fluid of a patient with adenocarcinoma of the colon. In spite of showing tumorigenicity in nude mice after subcutaneous injections, anchorage-independent clonal growth in soft agar, and invasion in the chick embryo skin, the Colo 205 cells failed to metastasize to the lung or liver after intrasplenic injections. The effects of interferon, and interferon in combination with 5-fluorouracil (5-FU), on tumor formation in the spleen, were studied. The combined interferon- and 5-FU-treated animals displayed a significant difference from the controls in the generation of spleen tumors. This combination may possess potentially useful applications in the treatment of solid tumors such as those in the colon and rectum.

Adenocarcinoma↗
PubMed1991

A specific cell surface glycoconjugate controlling cell motility: evidence by functional monoclonal antibodies that inhibit cell motility and tumor cell metastasis.

The biochemical basis of cell motility has been viewed as a complex process involving cell surface membrane proteins, integrin receptors, growth factors and their receptors, and cytoskeletal components [Rosen & Goldberg (1989) In Vitro 25, 1079]. The possible involvement of glycoconjugates at the cell surface in controlling cell motility has not been systematically investigated. We addressed this question using functional monoclonal antibodies (MAbs), which inhibit cell motility and the metastatic potential of tumor cells, as probes. Two such MAbs, derived from two independent processes of immunization and selection, were found to directed to a common specific carbohydrate structure, Fuc alpha 1----2Gal beta 1----R. MAb MIA-15-5 was established after immunization of mice with small cell lung carcinoma line PC7 and selected on the basis of inhibition of U937 and HEL cell migration. MAb MIA-22-20 was established after immunization with lung adenocarcinoma line MAC-10 and selected on the basis of inhibition of MAC-10 cell migration. These two MAbs were both IgM and were consistently reactive with the Fuc alpha 1----2Gal beta 1----R structure, regardless of the identity of the R group. Various other anti-H MAbs, specific to carrier isotype, did not affect cell motility. MAb MIA-15-5 reacted with 30-40% of high-metastatic variant BL6 of mouse melanoma B16 line but with only less than 5% of low-metastatic variant F1. Metastatic deposition to lung after injection of BL6 cells was inhibited if MAb MIA-15-5 was injected within 3 h but was not inhibited by injection of other anti-H antibodies under the same conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Carcinoma-associated perisinusoidal laminin may signal tumour cell metastasis to the liver.

The perisinusoidal space of the liver shows extensive modulation of the extracellular matrix in response to various pathological conditions. We studied perisinusoidal laminin expression immunohistochemically using polyclonal and monoclonal antibodies in 110 human liver specimens obtained at autopsy. In normal adult liver the perisinusoidal spaces contained only minimal amounts of immunoreactive laminin. In 86% of patients dying from cancer with liver metastasis, however, a distinct increase in the amount of perisinusoidal laminin could be demonstrated. The perisinusoidal space also contained laminin in cancer patients without liver metastasis. In 3 cases of leukaemia sinusoids were laminin negative. In cirrhosis and chronic passive congestion there was, as expected, laminin immunoreactivity in the perisinusoidal space. The results obtained using polyclonal antibodies against laminin were confirmed using chain-specific monoclonal antibodies against B2 laminin. In an ex vivo assay, viable tumour cells (Panc-1 and clone A) were found to bind with remarkable specificity to frozen sections of liver tissue containing perisinusoidal laminin as opposed to liver tissues without laminin. We suggest that this perisinusoidal laminin may directly on indirectly mediate tumour cell metastasis to the liver.

Carcinoma↗
PubMed1991

Possible role of cell cycle-dependent morphology, geometry, and mechanical properties in tumor cell metastasis.

Studies that examine the shear- and abrasion-sensitivity of proliferating cells are important in order to understand the behavior of hybridoma cells in bioreactor culture and metastasizing cancer cells in the bloodstream. Little is known about the link between morphology, structure, and mechanical properties of a given cell line, especially with respect to variations throughout the cell cycle. In our experiments with GAP A3 hybridoma cells, distinct cell morphologies were identified and correlated with phases of the cell cycle by video microscopic observation of synchronized cells, and of individual cells that were followed throughout their cell cycle. Micropipet manipulation was used to measure the geometrical (cell volume) and mechanical (apparent cell viscosity) properties of single cells. As the cell cycle progressed at 37 degrees C, an increase in cell volume from 1400 microns 3 to 5700 microns 3 was accompanied by an increase in apparent cell viscosity from 430 poise to 12,000 poise, consistent with an accumulation of more cytoplasmic material in the "older" cells. Hybridomas are representative of the various leukemias derived from hemopoietic cells, and even though as a whole, they appeared to be rather shear-insensitive, the wide range of property values demonstrates that a given cell line cannot be characterized by a single value for any one property, and that properties must be related to the cell cycle when considering proliferating cells. It is interesting to see if distinct stages in the metastatic sequence of events might correlate with any of these physical features of the cell cycle, irrespective of cell type or cell line. For example, the cytokinetic doublet could represent a fragile structure that may fail and produce cell death under fluid-shear conditions that would not affect the cells at any other stage in the cell cycle. Identifying such cell cycle-dependent features in metastasizing cancer cells could lead to a better understanding of the metastatic process and to possible clinical treatments directed at making cells more shear- and abrasion-sensitive, and therefore, more likely to be killed by the natural hydrodynamic forces of the circulatory system.

Biomechanical Phenomena↗
PubMed1976

Biochemical analysis of cell adhesion to a substratum and its possible relevance to cell metastasis.

The evidence is reviewed that two types of cell attachment occur, depending upon the presence or absence of serum in the medium. In the absence of serum, attachment has many characteristics of a nonphysiological process. In the presence of serum, attachment occurs as a series of steps: adsorption of serum components onto the substratum, contact between the cell and substratum, initial attachment, and progressive attachments leading to cell spreading. Although there is a close interdependence of these events, they could be experimentally distinguished. Studies are reported indicating that cell spreading requires the adsorption of a specific serum glycoprotein onto the substratum surface. The relationship between cell adhesiveness and the altered behavior of malignant cells is discussed.

Animals↗
PubMed1987

Mechanisms of tumour cell metastasis.

Abercrombie and his colleagues have accumulated evidence that changes in the heterotypic contact-inhibition response are largely responsible for the invasiveness of cells, at least in culture. We have identified a 37,000 Mr protein on the surface of mouse fibrosarcoma cells that is involved in their in vitro invasion. Blocking this protein with specific antibodies inhibits the invasion of chicken heart fibroblasts by the tumour cells and normal heterotypic contact inhibition is restored. These results are presented in the general framework of metastatic mechanisms and we review a selection of more recent studies aimed at describing the metastatic phenotype in molecular terms.

Animals↗
PubMed1992

[The relationship between metastatic phenotype and steady expression of BGC-Ha-ras oncogene from metastasis cell lines in nude mice (abstract)].

NIH/3T3 cells transformed by activated BGC-Ha-ras (6.6 kb) with a point mutation at codon 12 were able to induce tumor in nude mice with lung metastasis. The metastatic phenotype seemed stable in vivo metastasis assay. After two round subculture of the successively induced metastasis foci, two cell lines, GCM-1/3T3 and GCM-2/3T3, were established. In Southern blot analysis it was found that the bands from GCM-1/3T3 and GCM-2/3T3 were the same. Based on Southern analysis and polymerase chain reaction-restriction fragment length polymorphism (PCR-RPLF), it was proved that the activated c-Ha-ras (6.6 kb) existed all along in the genomes of the transformed and metastatic culture cells. Amplification and over-expression of activated c-Ha-ras were shown by DNA and RNA dot blot hybridization in transformed and metastatic culture cells. The metastatic phenotype might be related to the existence and steady expression of the point mutated ras.

Animals↗
PubMed1985

Analysis of mammary tumour cell metastasis and release of bound n-acetylneuraminic acid.

A tumour model consisting of the highly metastatic mammary 13762 parental line, the non-metastatic and 6-thioguanine-resistant (TgR) variant line, and two TgR revertant lines (TgRrev, TgRrevM) that were occasionally metastatic, were used to determine whether the release of N-acetylneuraminic acid (NANA) was related to tumour metastasis. For comparative purposes, the occasionally metastatic R3230AC and the nonmetastatic DMBA8 tumour lines were studied. The NANA was considered to be in bound form, because acid hydrolysis was required to release it for high-pressure liquid chromatographic analyses. Sera of animals bearing the 13762 and R3230AC tumours had high levels of bound NANA. No differences were found in serum NANA levels in animals bearing metastatic or non-metastatic R3230AC tumours. Low levels of bound NANA were found in animals bearing the other tumour lines regardless of whether metastasis occurred or not. The experiments in vitro substantiated the in vivo findings. The phenotypic expression of bound NANA shedding did not correlate well with metastatic potential of the mammary tumour line. Our analyses suggest that this phenotypic marker cannot be used as a reliable indicator of metastasis.

Animals↗
PubMed1985

Tumor cell metastasis and surface neutral proteinase: effects of antimetastatic and antitumor drugs.

The levels of a trypsin-like neutral proteinase present on tumor cell surface (SNP) have been determined in P388, L1210, TLX5 leukemias, and in two lines of Lewis lung carcinoma having different metastatic potential. No correlation between metastatic potential and SNP levels of the tumor lines examined has been observed, and metastasis depression by antimetastatic and antineoplastic drugs was not accompanied by SNP inhibition. These data seem to support the view that metastatic potential is not necessarily related to tumor proteinase levels.

Animals↗
PubMed1986

Tumor cell metastasis.

Local tissue invasion and the formation of metastatic lesions are characteristic properties of many malignant tumors. The formation of metastases is a complex process involving the passage of tumor cells from the site of the primary bulk tumor through successive connective tissue barriers, ultimately resulting in the growth of secondary tumor cell colonies in distinct target organ locations. At many stages in the metastatic process, tumor cells interact with multiple components of the extracellular matrix. Recently, the importance of basement membrane as a barrier to invasive cells has been recognized. In the course of the transition from in situ to invasive carcinoma, normal or dysplastic epithelial cells residing on a basement membrane are replaced by neoplastic cells which subsequently invade the basement membrane and enter the underlying stroma. Once in the stroma, tumor cells can then penetrate the walls of blood vessels or the lymphatic system and enter into the circulation. Circulating tumor cells next arrest in the lumina of small vessels, invade the vessel wall, and leave the circulation. These cells are now directly exposed to the extracellular matrix of a target organ where they may grow to form secondary tumors. Throughout the metastatic process tumor cells are thus in contact with, and are potentially responsive to, various components of the extracellular matrix. This review provides a survey of the recent advances in our understanding of the interactions of metastatic tumor cells with the extracellular matrix. Specifically, the role of basement membrane as a barrier to metastatic tumor cells is examined.

Animals↗
PubMed1987

Diets rich in fish oil cannot control tumor cell metastasis.

Rats fed diets containing different amounts of polyunsaturated fatty acids either of the n-3 or n-6 type, received cultured, syngeneic mammary tumor (BN472) cells intravenously. Animals were sacrificed 2 weeks after tumor inoculation, and the number of pulmonary tumor foci was counted. No significant differences in the number of metastatic foci were observed between the dietary groups. Prostaglandin measurements in the supernatant of tumor cells cultured in vitro showed that the tumor cells could produce thromboxane A2. Many investigators connected this tumor synthesis capacity with tumor metastatic activity. Yet in our study, diets rich in menhaden oil, with the known capacity to inhibit thromboxane synthesis, could not control tumor metastasis in this particular tumor model.

Adenocarcinoma↗
PubMedDate not supplied

Multi-step cascade of tumor cell metastasis.

The most life-threatening aspects of the oncogenic process are invasion and metastasis. Even though the clinical significance of such expression of the malignant phenotype has been well appreciated, advances in understanding the molecular mechanisms involved in metastasis have been painstakingly slow. To tackle this complex, multi-step problem, investigators have separated invasion and metastasis into a series of defined, sequential steps, and focused on one step at a time. Efforts combining the disciplines of cell biology, protein biochemistry, and molecular genetics have resulted in a surge of new information, suggesting novel strategies for prognosis and therapy of metastatic cancer.

Animals↗