Adhesion Tumor-cell induced

Interactions between tumor cells and platelets can be analyzed by different methods. The ability of tumor cells to induce platelet aggregation ( tumor cells induced platelet aggregation TCIPA) is evaluated by the turbidometric assay (Menter et al., 1987 Watanabe et al., 1988 Sugimoto et al., 1991 Tang et al., 1993 Belloc et al., 1995). Besides, the ability of tumor cells to bind platelets can be evaluated by the classic adhesion assay (see below). 

Hyaluronic acid may be important in permitting tumor cells to migrate through the EGM. Tumor cells can induce fibroblasts to synthesize greatly increased amounts of this GAG, thereby perhaps facifitating their own spread. Some mmor cells have less heparan sulfate at their surfaces, and this may play a role in the lack of adhesiveness that these cells display. 

The increased expression of adhesion molecules by the endothelium may activate polymorphonuclear neutrophils (PMN) in rabbits [72], During endotoxic shock, activated PMNs release their granule content and secrete both proinflammatory and cytotoxic molecules. Pickaver et al. [73] were the first to show PMN cytotoxicity against tumor cells. We showed that PMNs are toxic for PROb colon tumor cells [74] in BDEX rats. In vivo, PMNs have been implicated in the Schwartzman reaction [75], and may be involved in LPS-induced tumor necrosis. PMNs, when activated by LPS, synthesize and release NO. The role of NO in tumor growth will be discussed later. The decrease in tumor growth after intradermal injections of LPS is attributed to the induction of TNF-a secretion by PMNs both in intradermal tumors (Meth A sarcoma in BALB/c mice, MH-134 hepatoma in C3H/He mice, Lewis Lung carcinomas in C57BL/6 mice) and pulmonary Meth A metastases [76,77],... 

In vitro platelet-tumor cell adhesion assay If the ability of tumor cells to induce platelet aggregation has a prominent role in metastasis formation, it could be expected that its inhibition by specific drugs would reduce the amount of metastases produced by tumor cells with a pronounced TCIPA activity. 

Hakomori, S. (1994). Novel endothelial cell activation factor(s) released from activated platelets which induce E-selectin expression and tumor cell adhesion to endothelial cells a preliminary note. Biochem. Biophys. Res. Conun. 203, 1605-1613. 

Lauri, D., Needham, L., Martin-Padura, I. and Dejana, E. (1991). Tumor cell adhesion to endothelial cells ELAM-1 as an inducible adhesive receptor specific for colon carcinoma cells. J. Natl. Cancer Inst. 83, 1321-1324. 

Almost in vivo studies have been carried out on the ginsenosides (Fig. (1)). The /.v.(10-100 gg/mouse) or p.o. (100-1000 gg/mouse) multiple administration of ginsenoside-Rb2, 20 (R)- and 20 (S)-ginsenoside-Rg3 (Fig. (1)) isolated from red ginseng was demonstrated to inhibit lung metastasis produced by B16-BL-6 melanoma and colon 26-M3.1 carcinoma cells in syngeneic mice (Table 1) [18, 19]. The mechanism of their antimetastatic effect was related to the inhibition of the invasion and adhesion by tumor cells and also to the suppression of tumor-induced angiogenesis [18, 19]. 

Resveratrol has been shown to inhibit proliferation, induce differentiation, and enhance the expression of adhesion molecules (GDI la, GDI lb, GDIS, GD54) in a variety of myeloid leukemia cell lines [144]. The inhibitory effect of resveratrol on cell survival and proliferation of human breast cancer cells was shown to be estrogen receptor dependent [145]. Other studies indicated that it was very effective in inhibiting growth of 4T1 breast cancer cells in culture but had little effect on 4T1 tumor cell growth in mice [146]. In stark contrast, resveratrol was tested against mammary tumors induced by 7, 12-dimethylbenz(a)anthracene (DMBA) in rats [147]. In this case, reductions in incidence, multiplicity, and latency period of tumor development were observed. Additional... 

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