Through the conversion of low-energy NIR light (700–1000 nm) into high-energy ultraviolet/visible light UCNPs achieve greater tissue penetration depth (up to several centimeters) while minimizing phototoxicity and tissue damage that typically results from traditional ultraviolet/visible light excitation. The blue/green light produced by UCNPs when excited at 980 nm NIR helps activate photosensitizers and addresses traditional PDT's visible light penetration problem that limits depth to less than 1 cm.
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UCNPs provide solutions to major cancer treatment obstacles while addressing existing challenges.
Currently, traditional PDT faces two major bottlenecks: Visible light fails to reach deep tumors because of shallow penetration depth and photosensitizers face challenges because hydrophobic ones like zinc phthalocyanine ZnPc aggregate and become inactive while lacking targeting capabilities.
UCNPs can break through limitations: NIR excites UCNPs to emit high-energy photons which activate photosensitizers for reactive oxygen production (e.g., singlet oxygen) that kills deep cancer cells while tumor targeting is enabled through surface modifications like folic acid and peptide ligands enhancing treatment precision.
Through fluorescence resonance energy transfer or long-range FRET photosensitizers like ZnPc, Ce6 and TCPP receive high-energy photons from UCNPs to create reactive oxygen species effectively. For example: Folate receptor-modified nanoparticles loaded with Ce6 demonstrate significant mouse colon cancer growth inhibition after 980 nm laser activation and UCNPs containing dual photosensitizers increase singlet oxygen production efficiency.
Multifunctional core-shell structures are used. The UCNPs@AgBiS2 nanoparticles demonstrate combined photothermal and photodynamic therapy effects which enable successful tumor destruction in the 4T1 breast cancer model.
Stimulus-responsive release is also being used. The UCNP@PAA-DNA nanoparticles generate increased reactive oxygen when enzyme triggers activate them within the tumor microenvironment.
Targeted Delivery: Improving Therapeutic Specificity
The targeting ability of upconversion nanoparticles (UCNPs) towards pancreatic cancer cells that express elevated levels of EGFR can be enhanced through surface modification with EGFR antibodies like cetuximab or ligands which leads to more effective drug delivery and reduced systemic toxicity. For example: Research demonstrates that gold nanoparticles modified with cetuximab bind pancreatic cancer cells with elevated EGFR expression such as PANC-1 and AsPC-1 and effectively reduce tumor growth in laboratory and animal models.
Chitosan nanocarrier: EGFR-targeted chitosan nanoparticles loaded with gemcitabine (such as G-GC-Dox) show 40% greater uptake in SW1990 cells compared to non-targeted carriers while reducing cell survival to 18.26% in 48 hours demonstrating effective targeting and tumor suppression.
Polycyanoacrylate n-butyl ester nanoparticles: The tumor inhibition rate of drug-loaded nanoparticles coupled with EGFR monoclonal antibodies in the nude mouse pancreatic cancer model is significantly higher than that of the control group, and the tumor tissue fluorescence shows that the targeted enrichment reaches a peak within 5 hours.
NaGdF4:Yb/Er@SiO2 nanoparticles can achieve MRI/fluorescence imaging and photodynamic therapy (PDT) by modifying the surface of EGFR antibodies, providing the possibility for real-time monitoring and precision treatment.
Chlorotoxin (CTX) can target glioma cell membrane proteins (such as matrix metalloproteinase-2). After modification on the surface of UCNPs: radiosensitizing nanoparticles (GNPs) co-modified with insulin and CTX successfully penetrated the blood-brain barrier in a mouse model, inhibited the growth of glioblastoma and prolonged survival. CTX-modified nanoparticles reduce damage to normal brain tissue by binding to tumor cells with high expression of EGFR.
Combined Treatment Strategy: Synergistic Enhancement of Efficacy
UCNPs co-loaded photosensitizers (such as Ce6) and chemotherapeutic drugs (such as doxorubicin), and triggered dual treatment by near-infrared light (NIR): mesoporous titanium dioxide shell loaded with doxorubicin, synchronously released drugs and activated photosensitizers under NIR irradiation, and in vitro experiments showed that the cancer cell killing rate increased by more than 50%.
Overcoming drug resistance: Combined therapy can inhibit DNA repair mechanisms and reverse pancreatic cancer cell resistance to gemcitabine.
NaGdF4:Yb/Er nanoparticles have both MRI contrast and PDT functions: Gadolinium (Gd3+) enhances MRI contrast, while Yb/Er ions achieve upconversion luminescence, tracking tumor changes in real time during treatment.
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