Nanospacecraft Helps Cancer Therapies Land on Specific Target ACS_AMI
By Dr. Priyom Bose, Ph.D.Oct 6 2022Reviewed by Megan Craig, M.Sc. Conventional chemotherapeutics kill both cancerous and healthy cells and cause several side effects in patients. The negative effects limit the maximum tolerated drug dose, compromising its optimal therapeutic efficacy.
Limitations of Conventional Chemotherapeutics for Cancer Therapy In the past few decades, conventional chemotherapeutics have been used as the first line of standard treatment for a wide range of malignancies. One of the commonly used drugs is doxorubicin , which exhibited desirable therapeutic efficacy against malignancies. Mechanistically, this drug interferes with nucleic acid synthesis in cancerous cells.
Several human cancers have been linked with mitochondrial dysfunctions, such as insensitivity to anti-growth signals, uncontrolled cell proliferation, decreased autophagy, and enhanced anabolism. The malignant properties of cancer cells are associated with a high reactive oxygen species level, which can promote drug resistance. Recently, mitochondria have been considered to be a potential target for anticancer drugs, including Dox.
Although nanocarriers can target tumor cells, the majority of them cannot transport antitumor drugs into subcellular organelles . To overcome this limitation, there is a need to develop a targeted drug-delivery system that can deliver anticancer therapeutics into specific cellular organelles. GM-NSC is a nanocomposite containing Au-NPs, surrounded by dense multilayers of DNA crowns that are self-assembled from DNA tetra in an orderly fashion. Each tetrahedral DNA structural unit was equipped with three functional components, namely, a hidden mitochondria-targeting triphenylphosphonium , an explosive bolt , and a cancer cell-targeting aptamer pointing toward the outer environment. E-bolt has been assembled from the Lock strand, DNAzyme, and cleavage substrate.
Dox-loaded GM modified with TPP was able to precisely penetrate mitochondria and promote the mitochondrial accumulation of Dox, which ultimately damaged mitochondria by ROS generation and lowering of mitochondrial membrane potential. Subsequently, cytochrome c was released into the cytoplasm, which activated apoptosis-related enzymes caspase-9 and caspase-3. These activated enzymes triggered a cascade of molecular events causing tumor cell apoptosis.
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