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Barbieri, V.

Publications and source records attributed to Barbieri, V..

2 recordsLinked to original sources

Transferrin Receptor 1-targeted polymersomes therapy for Colorectal Cancer

Colorectal cancer (CRC) is a major global health concern, ranking among the most common cancers and the second leading cause of cancer-related deaths. The high mortality associated with CRC is attributed mainly to difficulties in early detection and the lack of effective targeted therapies. The Transferrin receptor 1 (TfR1) is particularly attractive as a therapy target given its notable overexpression in tumor cells, particularly in CRC. This study explored the potential of a polymeric nanoparticle (POs)-based drug delivery system targeting TfR1 to improve the precision and efficacy of CRC treatment. For this study, we used three human colorectal cancer cell lines (SW480, HT-29, and HCT116), a healthy human intestinal epithelial cell line (hIECs), and a murine CRC cell line (MC38). We first engineered POs composed of poly (ethylene glycol) (PEG) and poly (lactic acid) (PLA), functionalized with the T7 peptide to enhance their specificity for TfR1-expressing cells. Targeting efficiency of these POs was assessed across all cell lines by evaluating the cellular uptake using flow cytometry. Upon establishing the optimal formulation for these NPs for TfR1-targeting, we encapsulated doxorubicin (DOX) to evaluate their therapeutic potential. Both in vitro and in vivo studies were performed to assess the efficacy of these DOX-loaded TfR1-targeted POs. In vitro studies demonstrated selective delivery of DOX to CRC cells, suggesting a marked reduction in off-target effects. In vivo studies in a murine model of CRC further supported these findings, showing that DOX-loaded TfR1-targeted POs significantly improved survival rates and reduced tumor growth compared to free DOX or PBS treatments. These results highlight the promise of TfR1-targeted POs as a precise strategy for CRC therapy, offering enhanced treatment efficacy while reducing systemic toxicity. This novel approach could lead to the development of more targeted and less harmful cancer treatments. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=76 SRC="FIGDIR/small/639871v1_ufig1.gif" ALT="Figure 1"> View larger version (26K): org.highwire.dtl.DTLVardef@1714603org.highwire.dtl.DTLVardef@1ab7f15org.highwire.dtl.DTLVardef@245f6eorg.highwire.dtl.DTLVardef@1f56f75_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIT-7 peptide-functionalized polymersomes exhibit high binding affinity to CRC cell lines C_LIO_LIDoxorubicin-loaded T7-peptide polymersomes effectively suppress tumor growth and prolong survival in vivo C_LIO_LITargeted Doxorubicin delivery via T7-peptide polymersomes minimizes toxicity to healthy tissues C_LI

cancer biology↗

A tissue- and organ-based cell biological atlas of obesity-related human genes and cellular pathways

Over the last decades, several features of obesity have been identified at behavioral, physiological, endocrine and genomic levels, and they have revealed the complexity of the disease; obesity results from a combination of genetic predisposition, endocrine disorders, and dysregulation of both food intake and energy expenditure. This complexity makes the development of new therapeutic regimens challenging and bariatric surgery is still the treatment of choice for many obese patients. Given the need for noninvasive therapeutic intervention strategies, we sought to systematically study the biological manifestations of obesity in peripheral organs. We analyzed publicly available datasets of genes, genomic determinants, and levels of obesity-related hormones in the blood, using a combination of methodologies, including graph theory and dynamical modeling, that allow for the integration of different types of datasets. The analysis revealed tissue- and organ-specific metabolic impairments and potential new drug targets. All the data are organized into a tissue/organ-based subcellular-function atlas for human obesity. The data show that the complexity of the obesity arises due to the multiplicity of subcellular processes in different peripheral organs.

systems biology↗