scholarly journals Prediction of radiosensitivity in human bladder cell lines using nuclear chromatin phenotype

2006 ◽  
Vol 69A (10) ◽  
pp. 1077-1085 ◽  
Author(s):  
Nor F. Rajab ◽  
Declan J. McKenna ◽  
Jim Diamond ◽  
Kate Williamson ◽  
Peter W. Hamilton ◽  
...  
2000 ◽  
Vol 47 (2) ◽  
pp. 427-434 ◽  
Author(s):  
A Lityńska ◽  
M Przybyło ◽  
D Ksiazek ◽  
P Laidler

Expression as well as properties of integrins are altered upon transformation. Cell adhesion regulated by integrins is modulated by glycosylation, one of the most frequent biochemical alteration associated with tumorogenesis. Characterisation of carbohydrate moieties of alpha3beta1 integrin on the cultured human bladder carcinoma (T-24, Hu456, HCV 29T) and human normal ureter and bladder epithelium (HCV 29, Hu609) cell lines was carried out after an electrophoresis and blotting, followed by immunochemical identification of alpha3 and beta1 integrin chains and analysis of their carbohydrates moieties using highly specific digoxigenin-labelled lectins. In all the studied cell lines alpha3beta1 integrin was glycosylated although in general each subunit differently. Basic structures recognized in beta1 subunit were tri- or tetraantennary complex type glycans in some cases sialylated (T-24, HCV 29, HCV 29T) and fucosylated (Hu609, HCV 29T). Positive reaction with Phaseolus vulgaris agglutinin and Datura stramonium agglutinin suggesting the presence of beta1-6 branched N-linked oligosaccharides was found in cancerous cell lines (T-24, Hu456) as well as in normal bladder epithelium cells (Hu609). High mannose type glycan was found only in beta1 subunit from Hu456 transitional cell cancer line. On the other hand alpha3 subunit was much less glycosylated except the invasive cancer cell line T-24 where high mannose as well as sialylated tri- or tetraantennary complex type glycans were detected. This observation suggests that changes in glycosylation profile attributed to invasive phenotype are rather associated with alpha3 not beta1 subunit.


2000 ◽  
Vol 68 (10) ◽  
pp. 5869-5880 ◽  
Author(s):  
Melody Mills ◽  
Karen C. Meysick ◽  
Alison D. O'Brien

ABSTRACT Pathogenic Escherichia coli associated with urinary tract infections (UTIs) in otherwise healthy individuals frequently produce cytotoxic necrotizing factor type 1 (CNF1), a member of the family of bacterial toxins that target the Rho family of small GTP-binding proteins. To gain insight into the function of CNF1 in the development of E. coli-mediated UTIs, we examined the effects of CNF1 intoxication on a panel of human cell lines derived from physiologically relevant sites (bladder, ureters, and kidneys). We identified one uroepithelial cell line that exhibited a distinctly different CNF1 intoxication phenotype from the prototypic one of multinucleation without cell death that is seen when HEp-2 or other epithelial cells are treated with CNF1. The 5637 bladder cell line detached from the growth surface within 72 h of CNF1 intoxication, a finding that suggested frank cytotoxicity. To determine the basis for the unexpected toxic effect of CNF1 on 5637 cells, we compared the degree of toxin binding, actin fiber formation, and Rho modification with those CNF1-induced events in HEp-2 cells. We found no apparent difference in the amount of CNF1 bound to 5637 cells and HEp-2 cells. Moreover, CNF1 modified Rho, in vivo and in vitro, in both cell types. In contrast, one of the classic responses to CNF1 in HEp-2 and other epithelial cell lines, the formation of actin stress fibers, was markedly absent in 5637 cells. Indeed, actin stress fiber induction by CNF1 did not occur in any of the other human bladder cell lines that we tested (J82, SV-HUC-1, or T24). Furthermore, the appearance of lamellipodia and filopodia in 5637 cells suggested that CNF1 activated the Cdc42 and Rac proteins. Finally, apoptosis was observed in CNF1-intoxicated 5637 cells. If our results with 5637 cells reflect the interaction of CNF1 with the transitional uroepithelium in the human bladder, then CNF1 may be involved in the exfoliative process that occurs in that organ after infection with uropathogenic E. coli.


1977 ◽  
Vol 5 (3) ◽  
Author(s):  
Haruo Hisazumi ◽  
Lennart Andersson ◽  
V.Peter Collins

1996 ◽  
Vol 39 (1) ◽  
pp. 81-86 ◽  
Author(s):  
Olivier Pauwels ◽  
Michel Gozy ◽  
Paul Van Houtte ◽  
Jean-Lambert Pasteels ◽  
Ghanem Atassi ◽  
...  

Author(s):  
Rena Abulizi ◽  
Bo Li ◽  
Chuan-guang Zhang

Here, we characterized a new circRNA, named circ_0071662, which was downregulated in human bladder cancer tissues and cell lines, compared with matched adjacent normal tissues and normal bladder epithelial cells. Lower circ_0071662 level was observed in patients with advanced bladder cancer and was positively associated with poorer prognosis, including higher degrees of lymph node invasion and distal metastasis, and lower survival rate. Gain- and loss-of-functions showed that circ_0071662 suppressed cell proliferation and invasion in human bladder cell lines T-24 and J82. Bioinformatics analysis revealed that there are six binding sites of miR-146b-3p on circ_0071662 sequence, and pull-down assays demonstrated miR-146b-3p directly bound with circ_0071662. Moreover, circ_0071662 negatively regulated miR-146b-3p expression and positively regulated expression of miR-146b-3p target genes HPGD and NF2. Furthermore, miR-146b-3p could rescue the inhibition of cell proliferation and invasion caused by circ_0071662 overexpression. In conclusion, circ_0071662 suppresses bladder cancer cell proliferation and invasion by sponging miR-146b-3p.


Sign in / Sign up

Export Citation Format

Share Document