AI Article Synopsis
- Lung cancer is primarily linked to tobacco smoking through the production of harmful compounds called polycyclic aromatic hydrocarbons (PAHs), with the CYP1A1 gene playing a crucial role in their metabolism.
- The study investigates the use of RNA interference (RNAi) to inhibit the overactive CYP1A1 gene, employing lipid-coated microparticles to deliver siRNA that reduces CYP1A1 expression.
- Results indicate that targeting the CYP1A1 gene can suppress tumor growth in both cell cultures and animal models, suggesting that this liposome-based gene delivery method could be a promising strategy for lung cancer treatment in the future.
Article Abstract
The occurrence of lung cancer is linked with tobacco smoking, mainly through the generation of polycyclic aromatic hydrocarbons (PAHs). Elevated activity of cytochrome P4501A1 (CYP1A1) plays an important role in the metabolic processing of PAHs and its carcinogenicity. The present work aimed to investigate the role of CYP1A1 gene in PAH-mediated growth and tumor development in vitro and using an in vivo animal model. RNAi strategy was utilized to inhibit the overexpression of CYP1A1 gene using cationic liposomes generated using a lipid film-coated proliposome microparticles. Treatment of PAH-induced human alveolar adenocarcinoma cell line with cationic liposomes carrying CYP1A1 siRNA resulted in down regulation of CYP1A1 mRNA, protein as well as its enzymatic activity, triggering apoptosis and inhibiting multicellular tumor spheroids formation in vitro. Furthermore, silencing of CYP1A1 gene in BALB/c nude xenografts inhibited tumor growth via down regulation of CYP1A1 expression. Altogether, our findings showed that liposome-based gene delivery technology is a viable and stable approach for targeting cancer causing genes such as CY1PA1. This technology facilitated by the use of sugar particles coated with lipid films has demonstrated ability to generate anticancer effects that might be used in the future for therapeutic intervention and treatment of lung cancer.
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| http://dx.doi.org/10.1016/j.ijpharm.2019.04.078 | DOI Listing |
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