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Inhibition of angiogenesis- and inflammation-inducing factors in human colon cancer cells in vitro and in ovo by free and nanoparticle-encapsulated redox dye, DCPIP

Fadee G Mondalek1,4 email, Sivapriya Ponnurangam1 email, Janita Govind1 email, Courtney Houchen2 email, Shrikant Anant2,3 email, Panayotis Pantazis1,4 email and Rama P Ramanujam1,4 email

Swaasth, Inc., 800 Research Parkway Suite 350, Oklahoma City, OK 73104 - USA

University of Oklahoma Health Sciences Center, College of Medicine, Oklahoma City, OK 73104 - USA

University of Oklahoma Health Sciences Center, Department of Cell Biology, Oklahoma City, OK 73126 - USA

ADNA, Inc., Research Parkway Suite 350, Oklahoma City, OK 73104 - USA

author email corresponding author email

Journal of Nanobiotechnology 2010, 8:17doi:10.1186/1477-3155-8-17

Published: 15 July 2010

Abstract

Background

The redox dye, DCPIP, has recently shown to exhibit anti-melanoma activity in vitro and in vivo. On the other hand, there is increasing evidence that synthetic nanoparticles can serve as highly efficient carriers of drugs and vaccines for treatment of various diseases. These nanoparticles have shown to serve as potent tools that can increase the bioavailability of the drug/vaccine by facilitating absorption or conferring sustained and improved release. Here, we describe results on the effects of free- and nanoparticle-enclosed DCPIP as anti-angiogenesis and anti-inflammation agents in a human colon cancer HCT116 cell line in vitro, and in induced angiogenesis in ovo.

Results

The studies described in this report indicate that (a) DCPIP inhibits proliferation of HCT116 cells in vitro; (b) DCPIP can selectively downregulate expression of the pro-angiogenesis growth factor, VEGF; (c) DCPIP inhibits activation of the transcriptional nuclear factor, NF-κB; (d) DCPIP can attenuate or completely inhibit VEGF-induced angiogenesis in the chick chorioallantoic membrane; (e) DCPIP at concentrations higher than 6 μg/ml induces apoptosis in HCT116 cells as confirmed by detection of caspase-3 and PARP degradation; and (f) DCPIP encapsulated in nanoparticles is equally or more effective than free DCPIP in exhibiting the aforementioned properties (a-e) in addition to reducing the expression of COX-2, and pro-inflammatory proteins IL-6 and IL-8.

Conclusions

We propose that, DCPIP may serve as a potent tool to prevent or disrupt the processes of cell proliferation, tissue angiogenesis and inflammation by directly or indirectly targeting expression of specific cellular factors. We also propose that the activities of DCPIP may be long-lasting and/or enhanced if it is delivered enclosed in specific nanoparticles.


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