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MeSH Review

HT29 Cells

 
 
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Disease relevance of HT29 Cells

 

High impact information on HT29 Cells

  • The only receptor consistently detected was CXCR4 (fusin/LESTR), although HT-29 cells did not express mRNA for its ligand, stromal cell-derived factor (SDF-1alpha) [6].
  • Butyrate but not acetate or proprionate decreased basal and cAMP-stimulated bumetanide-sensitive K+ (86Rb) uptake in both HT29 cells and the Cl--secreting T84 line [7].
  • RESULTS: Clinically relevant concentrations of cisplatin, doxorubicin, mitomycin C, fluorouracil, or camptothecin enhanced Fas receptor expression on the plasma membrane of HT29 cells [8].
  • We also assessed the ability of UCN-01 to enhance the cytotoxicity of gamma irradiation in CA46 cells and human colon carcinoma HT-29 cells, both of which are mutant for p53 function [9].
  • TNF increased VCAM-1 expression to 4.2 times the vehicle-treated control levels (P < .05) on HT-29 cells and increased ICAM-1 expression on HT-29, LoVo, and SW-620 cells (8.4, 1.8, and 1.9 times vehicle control levels, respectively; P < .05 in each case) [10].
 

Chemical compound and disease context of HT29 Cells

  • For example, HT29 cells (alkyltransferase activity, 381 fmol/mg protein) exhibited a greater degree of enhancement when treated with O6-benzylguanine than SF767 (77 fmol/mg protein) and M19-MEL melanoma (36 fmol/mg protein) cells [11].
  • To test this hypothesis, we treated HT29 and SW620 human colon cancer cells with fluorodeoxyuridine under conditions that produced nearly complete inhibition of thymidylate synthase but which sensitized only the HT29 cells [12].
  • Cellular invasion induced by 10 ng/ml stem cell factor (EC(50) = 3 ng/ml) in HT29 cells was blocked by 1 micro M STI571 (IC(50) = 56 nM) and pharmacological inhibitors of several oncogenic signaling pathways, namely, phosphatidylinositol 3-kinase (LY294002), Rho GTPases (Clostridium botulinum exoenzyme C3 transferase), and Rho-kinase (Y27632) [13].
  • Taken together, these results suggest that suramin blocks HIV-1 infection in HT-29 cells because it binds to the V3 domain of gp120 and hence prevents the interaction between gp120 and the GalCer receptor [14].
  • 1-Deoxymannojirimycin (dMM), a specific alpha-mannosidase I inhibitor, completely blocks the conversion of Man9-8GlcNAc2 into Man7-5-GlcNAc2 in both differentiated and undifferentiated human adenocarcinoma HT-29 cells [15].
 

Biological context of HT29 Cells

 

Anatomical context of HT29 Cells

 

Associations of HT29 Cells with chemical compounds

  • HT-29 cells induced to differentiate by another signal, glucose deprivation, upregulated receptor content and response to toxin [25].
  • The effect of UCN-01 on the cytotoxicity of gamma irradiation in CA46 and HT-29 cells was determined by use of MTT (thiazolyl blue) and clonogenic (colony-forming) assays, respectively; a clonogenic assay was also used to measure the effect of UCN-01 on the cytotoxicity of cisplatin in transfected and nontransfected MCF-7 cells [9].
  • METHODS: A clinical phase I study of STZ followed by BCNU was designed to simulate conditions that produce maximal sensitization of CENU-resistant HT-29 cells in vitro [26].
  • In contrast, neither STa nor guanylin changed the uptake of taurine in HT-29 cells [27].
  • RESULTS: SN-38 and CPT were more cytotoxic than 9-AC and TPT, and CPT-11 was almost inactive toward HT-29 cells [28].
 

Gene context of HT29 Cells

  • NF-kappaB binding activity was unaltered by PI 3-kinase inhibition in HT-29 cells, in which TNF-alpha was shown to activate PI 3-kinase directly [29].
  • RESULTS: TNF-alpha and IL-1 beta dose-dependently induced IL-8 production in HT-29 cells [30].
  • IELs lysed more 51Cr-labeled HT-29 cells when cultured for 72 hours with IL-15 (48% +/- 3% at 25:1 effector-to-target ratio) than with IL-2 (27% +/- 3%) or IL-7 (12% +/- 2%) (P < 0.0001) [31].
  • When the antisense orientation of the VIP receptor clone was introduced into HT-29 cells, there was a 50% suppression of the specific binding of 125I-VIP and of the VIP-induced increase in cAMP level, relative to untransfected cells [22].
  • Mice bearing EGFR+ tumor cells lived significantly (P less than 0.001) longer when treated with TGF alpha-PE40 delta cys compared with saline-treated controls (median survival: A431 cells, 51.5 vs. 25.5 days; HT29 cells, 101 vs. 47.5 days) [32].
 

Analytical, diagnostic and therapeutic context of HT29 Cells

References

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  2. Anti-cell surface monoclonal antibodies which antagonize the action of VIP in a human adenocarcinoma cell line (HT 29 cells). Pichon, J., Hirn, M., Muller, J.M., Mangeat, P., Marvaldi, J. EMBO J. (1983) [Pubmed]
  3. Activation of AP-1 and of a nuclear redox factor, Ref-1, in the response of HT29 colon cancer cells to hypoxia. Yao, K.S., Xanthoudakis, S., Curran, T., O'Dwyer, P.J. Mol. Cell. Biol. (1994) [Pubmed]
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