158 POSTER Targeting bladder tumor cells in vivo and in the urine by a peptide identified using phage display

2006 ◽  
Vol 4 (12) ◽  
pp. 51
Author(s):  
B.-H. Lee ◽  
H.-Y. Hong ◽  
S.-J. Oh ◽  
E.-J. Lee ◽  
K. Wan ◽  
...  
2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 10071-10071
Author(s):  
T. Kwon ◽  
B. Lee ◽  
E. Yoo ◽  
S. Chung ◽  
Y. Park ◽  
...  

10071 Background: Bladder cancer is one of the most common tumors of genitourinary tract. Selective delivery of drugs to tumor tissues is important for effective tumor therapy. Here we identified a peptide targeting bladder tumor cells using phage display. Methods: Phage peptide library containing CX7C (C-cysteine and X-any amino acid residue) was based on T7 415–1b phage vector (Novagen). Tumor xenografts were prepared by subcutaneously injecting BALB/c Nu/nu female nude mice with HT-1376 bladder tumor cells. For a carcinogen-induced tumor model, Fischer 344 female rats were supplied ad libitum with tap water containing 0.05% N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) for 8 weeks. Results: A phage library containing CX7C random peptides was screened for selective binding to cells from human bladder tumor xenografts. Selected phage clones were individually evaluated for binding to cultured bladder tumor cells and for binding to cells from human tumor tissues of six patients. The peptide displayed by the most promising clone was synthesized and designated as Bld-1. Fluorescein-conjugated Bld-1 peptide showed selective binding to frozen sections of human bladder tumor tissues of three patients. In vivo tumor targeting was examined in a carcinogen-induced rat tumor model (n=20). When the fluorescent peptide was introduced into the bladder lumen, it selectively bound to tumor epithelium. Next, when the fluorescent peptide was intravenously injected into the tail vein, it homed to the bladder tumor, but was not detectable in normal bladder and control organs such as lung. Moreover, the fluorescent peptide bound to cells from urinary specimens of tumor patients (n=10), whereas little binding was observed in cells from healthy individuals (n=3). Conclusions: The Bld-1 peptide may be useful for targeting bladder tumor cells in vivo and in the urine. No significant financial relationships to disclose.


2007 ◽  
Vol 5 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Seung-Min Lee ◽  
Eun-Ju Lee ◽  
Hai-Yan Hong ◽  
Mi-Kyung Kwon ◽  
Tae-Hwan Kwon ◽  
...  

2016 ◽  
Vol 195 (4S) ◽  
Author(s):  
Kimberly Foreman ◽  
Alexandra Mitchell ◽  
Samuel White ◽  
Emil Bielecki ◽  
Maria Picken ◽  
...  

2016 ◽  
Vol 36 (1) ◽  
pp. 79-89 ◽  
Author(s):  
XIAOFENG YANG ◽  
FAN ZHANG ◽  
JUNQIAN LUO ◽  
JIANZHI PANG ◽  
SANHUA YAN ◽  
...  

2019 ◽  
Vol 2 (4) ◽  
pp. 83-98 ◽  
Author(s):  
André De Lima Mota ◽  
Bruna Vitorasso Jardim-Perassi ◽  
Tialfi Bergamin De Castro ◽  
Jucimara Colombo ◽  
Nathália Martins Sonehara ◽  
...  

Breast cancer is the most common cancer among women and has a high mortality rate. Adverse conditions in the tumor microenvironment, such as hypoxia and acidosis, may exert selective pressure on the tumor, selecting subpopulations of tumor cells with advantages for survival in this environment. In this context, therapeutic agents that can modify these conditions, and consequently the intratumoral heterogeneity need to be explored. Melatonin, in addition to its physiological effects, exhibits important anti-tumor actions which may associate with modification of hypoxia and Warburg effect. In this study, we have evaluated the action of melatonin on tumor growth and tumor metabolism by different markers of hypoxia and glucose metabolism (HIF-1α, glucose transporters GLUT1 and GLUT3 and carbonic anhydrases CA-IX and CA-XII) in triple negative breast cancer model. In an in vitro study, gene and protein expressions of these markers were evaluated by quantitative real-time PCR and immunocytochemistry, respectively. The effects of melatonin were also tested in a MDA-MB-231 xenograft animal model. Results showed that melatonin treatment reduced the viability of MDA-MB-231 cells and tumor growth in Balb/c nude mice (p <0.05). The treatment significantly decreased HIF-1α gene and protein expression concomitantly with the expression of GLUT1, GLUT3, CA-IX and CA-XII (p <0.05). These results strongly suggest that melatonin down-regulates HIF-1α expression and regulates glucose metabolism in breast tumor cells, therefore, controlling hypoxia and tumor progression. 


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