Abstract
BackgroundCurrent studies have demonstrated that DODAC/PHO-S (Dioctadecyldimethylammonium Chloride/Synthetic phosphoethanolamine) liposomes induces cytotoxicity in Hepa1c1c7 and B16F10 murine tumor cells, with a higher proportion than PHO-S. Therefore, our aim was to evaluate the potential of DODAC/PHO-S to elucidate the mechanism of cell death whereby the liposomes induces cytotoxicity in hepatocellular carcinoma Hepa1c1c7, compared to the PHO-S alone.MethodsLiposomes (DODAC/PHO-S) were prepared by ultrasonication. The cell cycle phases, protein expression and types of cell’s death on Hepa1c1c7 were analyzed by flow cytometry. The internalisation of liposomes, mitochondrial electrical potential and lysosomal stability were also evaluated by confocal laser scanning microscopy.ResultsAfter treatment with liposomes (DODAC/PHO-S), we observed a significant increase in the population of Hepa1c1c7 cells experiencing cell cycle arrest in the S and G2/M phases, and this treatment was significantly more effective to promote cell death by apoptosis. There also was a decrease in the mitochondrial electrical potential; changes in the lysosomes; nuclear fragmentation and catastrophic changes in Hepa1c1c7 cells. The liposomes additionally promoted increases in the expression of DR4 receptor, caspases 3 and 8, cytochrome c, p53, p21, p27 and Bax. There was also a decrease in the expression of Bcl-2, cyclin D1, CD90 and CD44 proteins.ConclusionThe overall results showed that DODAC/PHO-S liposomes were more effective than PHO-S alone, in promoting cytotoxicity Hepa1c1c7 tumor cells, activating the intrinsic and extrinsic pathways of programmed cell death.
Highlights
Current studies have demonstrated that DODAC/PHO-S (Dioctadecyldimethylammonium Chloride/ Synthetic phosphoethanolamine) liposomes induces cytotoxicity in Hepa1c1c7 and B16F10 murine tumor cells, with a higher proportion than PHO-S
DODAC/PHO-S liposomal formulation induces cell cycle arrest in G2/M The compounds were evaluated for their ability to induce changes in the cell cycle
The exposure time was determined by taking into account the results of the DODAC/PHO-S induces an increase in the number of apoptotic cells The Hepa1c1c7 cells were treated with PHO-S, DODAC/PHO-S (1:1) and DODAC (0.3–2.0 mM), for 12 h
Summary
Current studies have demonstrated that DODAC/PHO-S (Dioctadecyldimethylammonium Chloride/ Synthetic phosphoethanolamine) liposomes induces cytotoxicity in Hepa1c1c7 and B16F10 murine tumor cells, with a higher proportion than PHO-S. Our aim was to evaluate the potential of DODAC/PHO-S to elucidate the mechanism of cell death whereby the liposomes induces cytotoxicity in hepatocellular carcinoma Hepa1c1c7, compared to the PHO-S alone. Antineoplastic phospholipids (AFTs) and lipid precursors have emerged as a promising new classes of antitumor agents that do not target the DNA, they change the plasma membrane turnover, inducing cell death, with a high selectivity for cancer cell [3, 4]. Edelfosine, miltefosine, perifosine, erucylphosphocholine and erufosine, represent this new class of AFTs, structurally related antitumor agents [5,6,7].
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