Target carcinoma cells

Fishman P, Bar-Yehuda S, Rath-Wolfson L, Ardon E, Barrer F, Ochaion A, Madi L (2003) Targeting the A3 adenosine receptor for cancer therapy inhibition of prostate carcinoma cell growth by A3AR agonist. Anticancer Res 23(3A) 2077-2083 Fishman P, Bar-Yehuda S (2003) Pharmacology and therapeutic applications of A3 receptor subtype. Curr Top Med Chem 3(4) 463 169... 

Yamamoto, T. et al. Role of EGCG-targeted p57/KIP2 in reducing tumorigenicity of oral carcinoma cells and blocking c-jun N-terminal kinase-mediated apoptosis. Toxicol. Appl. Pharmacol. 224, 318, 2007. 

M. W. R. Robertson, M. Wang, G. P. Siegal, M. Rosenfeld, R. S. N. Ashford, R. D. Alvarez, R. I. Garver, and D. T. Curiel, Use of a tissue-specific promoter for targeted expression of the herpes simplex virus thymidine kinase gene in cervical carcinoma cells, Cancer Gene Ther. 5 331 (1998). 

Targeted delivery has also been used to investigate the structure of carbohydrates needed to obtain discrimination of cellular uptake between liver and tumor cells [184], A study was performed by doubly modifying BSA with both a fluorophore (via Lys isothiocyanate derivatization) and different fucose derivatives (via Tyr diazotization). Similar studies have used EDC-mediated coupling to also attach therapeutic agents for delivery to human embryonal carcinoma cells [185]. 

Merdan, T., Callahan, J., Petersen, H., Kunath, K., Bakowsky, U., Kopeckova, P., Kissel, T., and Kopecek, J. (2003) Pegylated polyethylenimine-Fab antibody fragment conjugates for targeted gene delivery to human ovarian carcinoma cells. 

Fig. 1. Effects of systemically delivered LErafsiRNA on Raf-1 expression in normal and tumor tissues, (a) Validation of target specificity of rafsiRNA in vitro. Human prostate carcinoma cells (PC-3) were treated with indicated concentration of the siRNA [Raf-1, B-Raf, or Scrambled (Scr)] and Oligofectamine according to supplier s instructions (Invitrogen Corp., Carlsbad, CA, USA) as described earlier (28). After 72 h,...

Considerable difference in the sensitivity to MK-2 and GG was found among the tumor cell lines used, with human leukemic cell lines (HL-60, ML-1, KG-1, K-562) the most sensitive and the human glioblastoma cell lines (T98G, U87MG) the most resistant. The sensitivity of the human oral squamous cell carcinoma cell lines (HSC-2, HSC-3, HSC-4) was intermediate. Consistent with previous reports [60,61], GG induced apoptosis in the most sensitive HL-60 cells, but not in the less sensitive HSC-4 cells. This suggested that the type of cell death induced (either apoptosis or non-apoptosis) may depend on the target cells. 

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