Background: Poly(lactic-co-glycolic acid) (PLGA) is a biodegradable and biocompatible polymer which is widely used as a matrix to incorporate therapeutic agents. The anticancer activity of targeted folate-modified docetaxel-loaded PLGA nanoparticles (F-NP-Doc) was studied in vitro. Methods: Nanoparticles were prepared by a single-emulsion solvent-evaporation technique and characterized by physico-chemical methods. Cell survival was measured by the MTT assay and the sulforhodamine B assay. Folate receptor α expression, particle uptake and apoptosis were assessed by flow cytometry. Results: Folate-modified docetaxel-loaded PLGA nanoparticles showed high anticancer activity in vitro against HeLa cervical carcinoma cells and MCF7 breast adenocarcinoma cells overexpressing folate receptors. Targeted F-NP-Doc nanoparticles were more active compared to free docetaxel and non-targeted NP-Doc nanoparticles; in contrast, the activity of targeted nanoparticles against human fibroblasts (negative control) was significantly lower. F-NP-Doc particles, like free docetaxel, induced apoptosis in cancer cells. F-NP-Doc, but not unmodified docetaxel-loaded PLGA nanoparticles, reversed multidrug resistance of MCF7 R breast adenocarcinoma cells. High antitumor activity of F-NP-Doc has also been proven in in vivo experiments. Conclusions: The summarized experimental data brought us to the conclusion that the incorporation of docetaxel into the targeted PLGA nanoparticles dramatically improves its selectivity against cancer cells.

No abstract

No abstract

No abstract

No abstract

No abstract

Using poly(lactic-co-glycolic) acid we developed a polymeric form of niclosamide (PFN) and investigated molecular mechanisms underlying its antitumor activity against human colorectal cancer cell lines (SW837, Caco-2, COLO 320 HSR). PFN was shown to be more cytotoxic against cancer cells and less cytotoxic against normal cells (human embryonic lung fibroblasts) as compared to niclosamide. Both niclosamide and its polymeric form caused mitochondrial damage (evaluated as a decrease in rhodamine 123 accumulation) and increased the levels of reactive oxygen species, particularly mitochondrial superoxide, resulting in the oxidative damage to biomolecules. Furthermore, niclosamide and PFN induced G0/G1 cell cycle arrest.

No abstract