1. Platelet-Membrane-Camouflaged Black Phosphorus Quantum Dots Enhance Anticancer Effect Mediated by Apoptosis and Autophagy.
- Author
-
Shang Y, Wang Q, Wu B, Zhao Q, Li J, Huang X, Chen W, and Gui R
- Subjects
- Animals, Breast Neoplasms metabolism, Breast Neoplasms pathology, Female, Humans, MCF-7 Cells, Mice, RAW 264.7 Cells, Xenograft Model Antitumor Assays, Antineoplastic Agents chemistry, Antineoplastic Agents pharmacokinetics, Antineoplastic Agents pharmacology, Apoptosis drug effects, Autophagic Cell Death drug effects, Blood Platelets, Breast Neoplasms drug therapy, Cell Membrane, Phosphorus chemistry, Phosphorus pharmacokinetics, Phosphorus pharmacology, Quantum Dots chemistry, Quantum Dots therapeutic use
- Abstract
Hederagenin (HED) has poor anticancer activity whose mechanism remains unclear and unsystematic. Free drugs for cancer treatment exhibit disadvantages such as poor targeting and efficacy. To address this problem, we constructed a nanoplatform of black phosphorus quantum dots (BPQDs) camouflaged with a platelet membrane (PLTm) carrying HED, termed PLT@BPQDs-HED. PLTm vesicles serve as a shell to encapsulate multiple high-efficiency drug-loaded nanocores, which can target tumor sites and significantly improve antitumor activity. Compared with free HED, this platform significantly reduced tumor cell viability and the mitochondrial membrane potential (MMP), while increasing the production of intracellular reactive oxygen species (ROS). The platform also significantly increased the amounts of terminal deoxyribonucleotide transferase mediated dUTP nick-end-labeling (TUNEL)-positive cells and decreased the number of Ki-67-positive cells. In addition, the platform upregulated proapoptotic factor Bax, downregulated the anti-apoptotic molecule Bcl-2, activated Caspase-9 and Caspase-3, and stimulated Cytochrome C release. Moreover, the platform promoted the formation of autophagosomes, upregulated Beclin-1, and promoted LC3-I conversion into LC3-II. This study demonstrated that the above platform significantly enhances tumor targeting and promotes mitochondria-mediated cell apoptosis and autophagy in tumor cells.
- Published
- 2019
- Full Text
- View/download PDF