Exploring the interplay between the TGF-β pathway and SLN-mediated transfection: implications for gene delivery efficiency in prostate cancer and non-cancer cells.

Solid lipid nanoparticles (SLN) are widely recognized for their biocompatibility, scalability, and long-term stability, making them versatile formulations for drug and gene delivery. Cellular interactions, governed by complex endocytic and signaling pathways, are pivotal for the successful application of SLN as therapeutic agents. This study aims to enhance our understanding of the intricate interplay between SLN and cells by investigating the influence of specific endocytic and cell signaling pathways, with a focus on the impact of the TGF-β pathway on SLN-mediated cell transfection in both cancerous and non-cancerous prostate cells. Here we conducted a systematic exploration of the intricate mechanisms governing the interactions between solid lipid nanoparticles and cells. By selectively manipulating endocytic and signaling pathways, we analyzed alterations in SLNplex internalization, intracellular traffic, and cell transfection dynamics. Our findings highlight the significant role of macropinocytosis in the internalization and transfection processes of SLNplex in both cancer and non-cancer prostate cells. Moreover, we discovered that the TGF-β pathway is an important factor influencing endosomal release, potentially impacting gene expression and modulating cell transfection efficiency. This study provides novel insights into the dynamic mechanisms governing the interaction between cells and SLN, emphasizing the pivotal role of TGF-β signaling in SLN-mediated transfection. With this, we shed new light on the mechanisms governing the interaction between cells and SLN and highlight the important role of TGF-β signaling in SLN-mediated transfection, affecting internalization, intracellular transport, and release of the genetic cargo. These findings contribute valuable knowledge for the optimization of SLN-based therapeutic strategies in prostate-related applications.&#xD.