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Colon carcinoma cells

KIRLIN w G, CAi J, DELONG M J, PATTEN E J and JONES D P (1999) Dietary compoimds that induce cancer preventive phase 2 enzymes activate apoptosis at comparable doses in HT29 colon carcinoma cells , JNutr, 129 1827-35. [Pg.64]

OITATE M, NAKAKI R, KOYABU N, TAKANAGA H, MATSUO H, OHTANI H, SAWADA Y (2001) TranSCellular transport of genistein, a soybean-derived isoflavone, across human colon carcinoma cell line (Caco-2). Biopharm Drug Dispos. 22 23-9. [Pg.182]

In culture, the human colon carcinoma cell hne Caco-2 spontaneously differentiates at confluency into polarized cells with enterocyte-like characteristics. The principle of this approach consists of following the passage of the compound of interest from the apical or lumen-like sides to the basolateral or lymph-hke sides of Caco-2 cells, thus following the absorption of the compound per se. One obhgate step for fat-soluble nutrients such as carotenoids to cross the intestinal barrier is their incorporation into CMs assembled in the enterocytes. Under normal cell culture conditions, Caco-2 cells are unable to form CMs. When supplemented with taurocholate and oleic acid, Caco-2 cells were reported to assemble and secrete CMs. ... [Pg.153]

The physiological role of the ICOR is not clear and may be heterogeneous in the various tissues. In the thick ascending limb of the loop of Henle this channel appears to serve as the exit for CP at the basal cell pole [16,65,66], This conductive mechanism, therefore, is required for the reabsorption of Na and CP by this segment of the nephron [16]. In the rectal gland of Squalus acanthias a very similar channel is utilized for Na" and CP secretion. In these latter cells the CP-channel is present in the luminal membrane and is controlled by cytosolic cAMP [15,56,71]. It has been claimed that this kind of channel is also responsible for the secretion of CP in the colonic crypt cell, in colonic carcinoma cells and in respiratory epithelial cells [17,19,20,22]. Recent data have cast some doubt on this concept ... [Pg.280]

CP-channels with smaller conductance have first been noted in the rectal gland of Squalus acanthias by ourselves and in the colonic carcinoma cell line HT29 [61,73]. Later these types of 5-15 pS CP-channels were also found in pancreatic ducts, A6-cells and many other cells [74,75]. It is now claimed that this kind of channel is much more relevant than the ICOR for the pathophysiology of cystic fibrosis [12]. [Pg.280]

CP-channels with even smaller conductance have been described for the lacrimal and other exocrine glands [76,77]. These channels have a conductance of 1-2 pS. Unlike the ICOR-channel they appear to be blocked by millimolar concentrations of furosemide [77]. Most recent and only partially published data from my own laboratory obtained with the above modified nystatin technique [50,133,134] indicate that the respiratory epithelial cells and colonic carcinoma cells possess these types of small CP channels, and that these channels are involved in hormonal regulation of CP-conductance (cf. section 5). These CP-channels are regulated by cytosolic Ca. Hormonally induced increases in cytosolic Ca lead to an abrupt increase in the probability of these small CP-channels being open, yet they have no effect on the ICOR-channel. Data of this kind reinforce that the physiological importance of these small CP-channels may have been grossly underestimated. [Pg.280]

Fig. 3. Cellular model for NaCl secretion ([16] e.g., in a colonic carcinoma cell). The symbols have the following meaning = (Na" + K )-ATPase (J = Na 2Cl K -cotransporter - = ion... Fig. 3. Cellular model for NaCl secretion ([16] e.g., in a colonic carcinoma cell). The symbols have the following meaning = (Na" + K )-ATPase (J = Na 2Cl K -cotransporter - = ion...
Meanwhile we have shown that the excision activation of ICOR channels is due to disinhibition [72]. The respective inhibitor, operationally named cytosolic inhibitor (Cl), is present in the cytosol of placenta trophoblast cells HT29- and Tg4-colonic carcinoma cells and RE cells of normal and CF patients. The molecule has an apparent molecular weight of 700-1 500 Da it is amphiphilic heat stable and not digested by trypsin, proteases, nucleotidases, lipases or amylase [72]. Burc-khardt, Fromter and their collaborators [114] have confirmed our results and extracted a similar or identical Cl from kidney cortex. [Pg.289]

Inhibition of DNA topo I activity in HCT 116 (human colon carcinoma) cells by CPT, CPT-11, SN-38, TPT, and EGCG (Table 8) ... [Pg.59]

Li A, Varney ML, Singh RK. Constitutive expression of growth regulated oncogene (gro) in human colon carcinoma cells with different metastatic potential and its role in regulating their metastatic potential. Clin Exp Metastasis 2004 21 571-579. [Pg.348]

Hidalgo, I. J. Kato, A. Borchardt, R. T., Binding of epidermal growth factor by human colon carcinoma cell (Caco-2) monolayers, Biochem. Biophys. Res. Commun. 160, 317-324 (1989). [Pg.279]

Royleanone, horminone, and acetyl horminone isolated from the roots of Salvia officinalis L. abrogated the survival of colon carcinoma cell Caco-2 and human hepatoma cell HepG2, cultured in vitro with induction of DNA breaks (48). [Pg.201]

Pinto, M. et al. (1983). Enterocyte-like differentiation an polarizationof the human colon carcinoma cell line Caco-2 in culture. Biol. Cell 47 323-330. [Pg.386]

Das, S.K., Hashimoto, T., Shimizu, K., and Kanazawa, K. 2005. Fucoxanthin induces cell cycle arrest at GO/ Gl phase in human colon carcinoma cells through up-regulation of p21WAFl/Cipl. Biochim Biophys Acta 30 328-335. [Pg.479]

Hoffmann, R, Ji, H., Moritz, R. L., Connolly, L. M., Frecklington, D. F., Layton, M. J., Eddes, J. S., Simpson, R. J. (2001). Continuous free-flow electrophoresis separation of cytosolic proteins from the human colon carcinoma cell line LIM 1215 a non two-dimensional gel electrophoresis-based proteome analysis strategy. Proteomics 1(7), 807. [Pg.239]

Hiribarren, A., Heyman, M., L Helgouac h, A. and Desjeux, J.F. (1993) Effect of cytokines on the epithelial function of the human colon carcinoma cell line HT29 cll9A. Gut 34, 616-620. [Pg.399]

Borchardt, R. T., Characterization of the human colon carcinoma cell line (Caco-2) as a model for intestinal epithelial permeability, Gastroenterology 1989, 96, 736-749. [Pg.120]

M. D., Kedinger, M., Triadou, N., Dussaulx, E., Lacroix, B., Simon-Assman, P., Happen, K., Fogh, J., Zweibaum, A., Enterocyte-like differentiation and polarization of the human colon carcinoma cell line Caco-2 in culture, Biol. Cell 1983, 47, 323-330. [Pg.121]

E., Brattain, M. G., Zweibaum, A., Epithelial polarity, villin expression, and enterocytic differentiation of cultured human colon carcinoma cells a survey of twenty cell lines, Cancer Res. 1988, 48, 1936-1942. [Pg.121]

Brandsch, M., Miyamoto, Y., Ganapathy, V., Leibach, F. H., Expression and protein C-dependent regulation of peptide/H+ co-transport system in the Caco-2 human colon carcinoma cell line, Biochem. J. 1994, 299, 253-260. [Pg.122]

Grasset, E., Pinto, M., Dussaulx, E., Z WEI BAUM, A., Desjeux, J.-F., Epithelial properties of human colonic carcinoma cell line Caco-2 electrical parameters, Am. J. Physiol. 1984, 247, C260-C267. [Pg.123]

Cell line human colon carcinoma cells... [Pg.288]

Schuetz, J. D., Modulators and substrates of P-glycoprotein and cytochrome P4503A coordinatefy up-regulate these proteins in human colon carcinoma cells, Mol. Pharmacol. 1996, 49, 311-318. [Pg.491]

Simpson RJ et al. Proteomic analysis of the human colon carcinoma cell line (LIM 1215] development of a membrane protein database. Electrophoresis 2000 21 1707-1732. [Pg.119]

Wang W, VanAlstyne PC, Irons KA, Chen S, Stewart JW and Birt DF. 2004. Individual and interactive effects of apigenin analogs on G2/M cell-cycle arrest in human colon carcinoma cell lines. Nutr Cancer 48(1) 106—114. [Pg.175]

Administration of Certain Proteases to Animals Enhances Metastasis. Administration of specific proteases to animals has been found to stimulate the production of metastasis. For example, in rabbits, administration of uPA has been found to enhance the metastasis of V2 carcinomas (K11), while in mice, exogenous uPA increased pulmonary metastasis from Lewis lung carcinomas (Tl). Also, infusion of thrombin into syngenic mice stimulated pulmonary metastasis from both colon carcinoma cells and melanoma cells (N5). This enhanced formation of metastasis in the presence of thrombin may result from increased tumor cell-platelet interaction in the presence of the protease (N5). [Pg.147]

C2. Cajot, J. F., Bamat, J., Bergonzelli, G. E., Kruithof, E., Medcalf, R. L., Tetuz, J., and Sordat, B., Plasminogen activator inhibitor type lisa potent natural inhibitor of extracellular matrix degradation by fibrosarcoma and colon carcinoma cells. Proc. Natl. Acad. Sci. U.S.A. 50, 4676-4684 (1990). [Pg.160]

In contrast to P-gp and the MRP proteins, the breast cancer resistance protein (BCRP) contains six transmembrane domains and only one ATP-binding domain. It was first cloned from the breast cancer cell line MCF-7 selected in doxombicin, in the presence of the P-gp inhibitor verapamil. It is found in many human tissues, such as the placenta, small intestine, colon, and liver [133], It is localized to the apical membrane of epithelial cells of the small intestine and colon and to the bile canalicular membrane in the liver and is involved in reducing intestinal uptake, increasing hepatobiliary excretion, etc., leading to diminished oral bioavailability. cDNA sequences identical to BCRP and named MXR and ABCP, respectively, were independently isolated from human colon carcinoma cells and human placenta [134], BCRP requires... [Pg.383]


See other pages where Colon carcinoma cells is mentioned: [Pg.743]    [Pg.100]    [Pg.291]    [Pg.46]    [Pg.58]    [Pg.95]    [Pg.98]    [Pg.320]    [Pg.96]    [Pg.164]    [Pg.174]    [Pg.92]    [Pg.359]    [Pg.123]    [Pg.118]    [Pg.379]   
See also in sourсe #XX -- [ Pg.29 , Pg.227 , Pg.234 ]




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