Colonic targeting colon cancer

Stein U, Arlt F, Walther W et al (2006) The metastasis-associated gene S100A4 is a novel target of p-catenin/ T-cell factor signaling in colon cancer. Gastroenterology 131 1486-1500... 

M. R. Ballestero, M. J. Monte, O. Briz, F. Jimenez, F. Gonzalez-San Martin and J. J. G. Marin, Expression of transporters potentially involved in the targeting of cytostatic bile-acid derivatives to colon cancer and polyps, Biochem. Pharmacol., 2006, 72, 729. 

O Brian CA, Ward NE, Gravitt KR, Gupta KP (1995) The tumor promoter receptor protein kinase C a novel target for chemoprevention and therapy of human colon cancer. Prog Clin Biol Res 391 117-120... 

Oh BY, Lee RA, Kim KH (2011) siRNA targeting Livin decreases tumor in a xenograft model for colon cancer. World J Gastroenterol 17 2563-2571... 

Shaheen RM, Davis DW, Liu W, et al. Antiangiogenic therapy targeting the tyrosine kinase receptor for vascular endothelial growth factor receptor inhibits the growth of colon cancer liver metastasis and induces tumor and endothelial cell apoptosis. Cancer Res 1999 59(21) 5412-5416. 

Koning, G. A., Kamps, J. A. A. M., and Scherphof, G. L. S. (2002), Efficient intracellular dehvery of 5-fluorodeoxyuridine into colon cancer cells by targeted immunoliposomes, Cancer Detection Prevention, 26,299-307. 

Many clinically relevant NSAIDs exert off-target effects unrelated to their ability to inhibit COX enzymes. For example, INDO and SS induce apoptosis of tumor cells and modulate y-secretase activity (15, 16). INDO also activates the nuclear transcription factor PPARy (17). The complexity of in vivo pharmacologic effects makes it a challenge to separate the contribution of COX inhibition from other effects in a given pharmacologic response. Thus, the removal of COX inhibitory activity by a minor modification, such as the removal of a methyl group, provides an opportunity to dissect COX-dependent and COX-independent effects of certain NSAIDs. In fact, DM-INDO and DM-SS activate PPARy in HCA-7 cells with dose responses similar to those of the parent drugs (14). Likewise, the rfei -methyl compounds exhibit potency similar to the parent compounds in their ability to induce apoptosis in RKO cells, a human colon cancer cell line, and to activate PPARy in cellular reporter assays. 

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