P Gasco

Publications (2)8.82 Total impact

• Article: Cholesteryl butyrate solid lipid nanoparticles inhibit the proliferation of cancer cells in vitro and in vivo models.

  R Minelli, S Occhipinti, C L Gigliotti, G Barrera, P Gasco, L Conti, A Chiocchetti, G P Zara, R Fantozzi, M Giovarelli, U Dianzani, C Dianzani
  [show abstract] [hide abstract]
  ABSTRACT: BACKGROUND AND PURPOSE: Cholesteryl butyrate solid lipid nanoparticles (cholbut SLN) can be a delivery system for the anti-cancer drug butyrate. We have previously shown that they inhibit adhesion of polymorphonuclear and tumor cells to endothelial cells and migration of tumor cells, suggesting that they may act as anti-inflammatory and antitumor agents. The aim of the research was to evaluate the activity of cholbut SLN on tumor cell growth using in vitro and in vivo models. EXPERIMENTAL APPROACH: Cholbut SLN were incubated with four tumor cell lines, and cell growth was analysed by assessing viability, clonogenic capacity and cell cycle. The effect on signalling was evaluated by western blot analysis of Akt expression. The in vivo anti-tumor activity was assessed using two models of PC-3 cell xenografts in SCID/beige mice. KEY RESULTS: Cholbut SLN inhibited tumor cell line viability, clonogenic activity, Akt phosphorylation, and cell cycle progression. Mice were injected i.v. with PC3-Luc cells and treated with cholbut SLN. In vivo optical imaging and histological analysis showed that no metastases were detected in the lungs of the treated mice. Mice were injected s.c. with PC-3 cells and treated with cholbut SLN when the tumor diameter reached 2 mm. Analysis of the tumor dimensions showed that treatment with cholbut SLN substantially delayed tumor growth. CONCLUSION AND IMPLICATIONS: These results demonstrated that cholbut SLN is effective in inhibiting tumor growth and suggest that this effect may partly involve inhibition of AKT phosphorylation, which adds another mechanism to the activity of this multifaceted drug.
  British Journal of Pharmacology 05/2013; · 4.41 Impact Factor
• Article: Cholesteryl butyrate solid lipid nanoparticles inhibit the adhesion and migration of colon cancer cells.

  R Minelli, L Serpe, P Pettazzoni, V Minero, G Barrera, Cl Gigliotti, R Mesturini, A C Rosa, P Gasco, N Vivenza, E Muntoni, R Fantozzi, U Dianzani, G P Zara, C Dianzani
  [show abstract] [hide abstract]
  ABSTRACT: BACKGROUND AND PURPOSE Cholesteryl butyrate solid lipid nanoparticles (cholbut SLN) provide a delivery system for the anti-cancer drug butyrate. These SLN inhibit the adhesion of polymorphonuclear cells to the endothelium and may act as anti-inflammatory agents. As cancer cell adhesion to endothelium is crucial for metastasis dissemination, here we have evaluated the effect of cholbut SLN on adhesion and migration of cancer cells. EXPERIMENTAL APPROACH Cholbut SLN was incubated with a number of cancer cell lines or human umbilical vein endothelial cells (HUVEC) and adhesion was quantified by a computerized micro-imaging system. Migration was detected by the scratch 'wound-healing' assay and the Boyden chamber invasion assay. Expression of ERK and p38 MAPK was analysed by Western blot. Expression of the mRNA for E-cadherin and claudin-1 was measured by RT-PCR. KEY RESULTS Cholbut SLN inhibited HUVEC adhesiveness to cancer cell lines derived from human colon-rectum, breast, prostate cancers and melanoma. The effect was concentration and time-dependent and exerted on both cancer cells and HUVEC. Moreover, these SLN inhibited migration of cancer cells and substantially down-modulated ERK and p38 phosphorylation. The anti-adhesive effect was additive to that induced by the triggering of B7h, which is another stimulus inhibiting both ERK and p38 phosphorylation, and cell adhesiveness. Furthermore, cholbut SLN induced E-cadherin and inhibited claudin-1 expression in HUVEC. CONCLUSION AND IMPLICATIONS These results suggest that cholbut SLN could act as an anti-metastastic agent and they add a new mechanism to the anti-tumour activity of this multifaceted preparation of butyrate.
  British Journal of Pharmacology 11/2011; 166(2):587-601. · 4.41 Impact Factor