Destroying Deep Lung Tumor Tissue through Lung-Selective Accumulation and by Activation of Caveolin Uptake Channels Using a Specific Width of Carbon Nanodrug

The main difficulty With current anticancer nanotherapeutics comes from the low efficiency of tumor targeting. Althoughniany strategies have been investigated, including cancer-specific antibody conjugation, lung tumors remain one of the invulnerable types of cancer that must be overcome in the near future. Meanwhile, despite their advantageous physiochemical properties, carbon nanotube structures are not considered safe medical drug delivery agents, but are considered a hazardous source that may cause pulmonary toxicity. However, high-aspect-ratio (width vs. length) nanostructures can he used as very efficient drug delivery agents due to their lung tissue accumulation property. Furthermore, selection of a specific width if the carbon nanostructures can activate additional caveolin uptake channels in cancer cells, thereby maximizing internalization of the nanodrug. The present study aimed to evaluate the therapeutic potential of carbon nanotube-based nanodrugs having various widths (10-30 nm, 60-100 mn, and 125-150 nm) as a delivery agent to treat lung tumors. The results of-the present study provided evidence that both lung tissue accumulation (passive targeting) and caveolin-assisted uptake (active targeting) can simultaneously contribute to the destruction of lung tumor tissues of carbon nanotube.