ArticleFrontiers in immunology2025
Selenium nanoparticle-delivered MDM2 inhibitor reactivates p53 and reprograms tumor immune microenvironment in colorectal cancer.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Exosomal circ_0050688 Shapes a Chemoresistant Microenvironment by Driving Spatial Resistance Spreading in Glioblastoma via the MDM2 Pathway.Biomolecules · 2026Article
- Nanomedicine delivery systems remodel the immunosuppressive microenvironment of colorectal cancer: synergistic strategies and mechanisms of targeted immune checkpoint inhibitors.Frontiers in immunology · 2026Review
- Nanoparticles that modulate immune cells - an important strategy for the future treatment of tumors.Frontiers in immunology · 2026Review
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Authors and funding
5 authors.
Funding
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Abstract
Background: Colorectal cancer (CRC) remains a major global health challenge, with limited immunotherapy efficacy in microsatellite stable (MSS) tumors that comprise ~85% of cases. The p53 tumor suppressor pathway, frequently inactivated through the mouse double minute 2 homolog (MDM2) overexpression in wild-type tumor protein 53(TP53) tumors, represents a promising therapeutic target for both direct antitumor effects and immune modulation. Methods: We developed selenium nanoparticles loaded with the MDM2-targeting peptide inhibitor MI (Se@MI) using a one-pot synthesis approach. The nanoparticles were characterized by transmission electron microscopy, dynamic light scattering, and UV-Vis spectroscopy. Results: Se@MI nanoparticles demonstrated uniform spherical morphology (45-50nm diameter) and displayed a positive zeta potential (+24.69 mV), indicative of favorable colloidal dispersibility. Enhanced cellular uptake (74.3% positive cells) and potent cytotoxicity (IC Conclusions: Se@MI represents a novel nanomedicine strategy that combines direct p53 pathway reactivation with immune microenvironment modulation. This dual mechanism of action offers a potential strategy to boost immunotherapeutic outcomes in colorectal carcinoma and may help overcome resistance mechanisms to immune checkpoint blockade.
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