Abstract
Prostate and breast cancer are the current leading causes of new cancer cases in males and females, respectively. Phosphatidylserine (PS) is an essential lipid that mediates macrophage efferocytosis and is dysregulated in tumors. Therefore, developing therapies that selectively restore PS may be a potential therapeutic approach for carcinogenesis. Among the nanomedicine strategies for delivering PS, biocompatible gold nanoparticles (AuNPs) have an extensive track record in biomedical applications. In this study, we synthesized biomimetic phosphatidylserine-caped gold nanoparticles (PS-AuNPs) and tested their anticancer potential in breast and prostate cancer cells in vitro. We found that both cell lines exhibited changes in cell morphology indicative of apoptosis. After evaluating for histone-associated DNA fragments, a hallmark of apoptosis, we found significant increases in DNA fragmentation upon PS-AuNP treatment compared to the control treatment. These findings demonstrate the use of phosphatidylserine coupled with gold nanoparticles as a potential treatment for prostate and breast cancer. To the best of our knowledge, this is the first time that a phosphatidylserine-capped AuNP has been examined for its therapeutic potential in cancer therapy.
Highlights
Phosphatidylserine (PS) is an essential lipid in eukaryotic cellular bilayer lipid membranes, and has structural and biochemical importance [1,2]
We found a red-shift for the PS-AuNP spectra compared to the AuNP, with a decrease in the surface plasmon resonance (SPR) peak and the formation of a broad band between
This suggests that PS-AuNP memembrane. It is usually present in the inner leaflet of the cellular membrane, diates cancer cell apoptosis that is recognized by normal phagocytic cells efferocytosis that remove and its exposure in the outer leaflet triggers macrophage
Summary
Phosphatidylserine (PS) is an essential lipid in eukaryotic cellular bilayer lipid membranes, and has structural and biochemical importance [1,2] It is the most abundant negatively charged glycerophospholipid in cell membranes, where it is actively maintained on the membrane’s inner leaflet by flippase enzymes [1]. PS is widely known for its emblematic participation in apoptosis, in which PS is externalized, upon losing membrane asymmetry These exposed PS interact with a set of extracellular serum proteins and PS receptors, triggering an array of biochemical and immunological responses that evoke recognition of the apoptotic bodies by phagocytes, which tag cells with an “eat me” signal for efferocytosis [1,3]. Recent data demonstrate that PS itself may play a more complex role in apoptosis than previously imaged [5], since
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