Journal
JOURNAL OF MATERIALS CHEMISTRY B
Volume 11, Issue 25, Pages 5856-5869Publisher
ROYAL SOC CHEMISTRY
DOI: 10.1039/d3tb00227f
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A calcium hydroxide/oleic acid/phospholipid nanoparticle with lipase/pH dual responsive delivery of Ca2+ and curcumin was developed for inducing cancer cell apoptosis by a combination of intracellular calcium overload and lactic acidosis elimination. The nanoparticle showed good performance and internalization by cancer cells, leading to activation of caspases and apoptosis through a mitochondrial-mediated pathway. The inhibition of apoptosis by lactic acid was eliminated by the nanoparticle, resulting in nearly complete apoptosis.
Intracellular calcium ions (Ca2+) influence the proliferation-apoptosis balance, and lactic acidosis is an innate feature of a malignant tumor. In this study, a calcium hydroxide/oleic acid/phospholipid nanoparticle [CUR-Ca(OH)(2)-OA/PL NP] with lipase/pH dual responsive delivery of Ca2+ and curcumin (CUR) was developed for inducing cancer cell apoptosis by a combination of intracellular calcium overload and lactic acidosis elimination. The nanoparticle showed a core-shell structure with some good performance, including an adequate nano-size, negative charge, good blood circulation stability, and non-hemolysis. MDA-MB-231 breast cancer cells exhibited a higher lipase activity than A549 human lung adenocarcinoma cells and L929 mouse fibroblasts by fluorescence analysis. CUR-Ca(OH)(2)-OA/PL NPs were highly internalized by MDA-MB-231 cells, intracellularly released CUR and Ca2+, triggered the activation of caspase 3 and caspase 9, and caused apoptosis by intracellular calcium overload via a mitochondrial-mediated pathway. Lactic acid of 20 mM inhibited the apoptosis of MDA-MB-231 cells depending on the glucose insufficiency level, but this inhibition could be eliminated by CUR-Ca(OH)(2)-OA/PL NPs, leading to nearly complete apoptosis. Herein, CUR-Ca(OH)(2)-OA/PL NPs are a potential killer of cancer cells with high lipase activity by a combination of intracellular calcium overload and lactic acidosis elimination.
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