Table 3.
Studies using magnetic nanoparticles (MNPs) for cancer theranostics.
| MNP (Particle Size) + Composition |
Treatment + Cancer Model | Results | Ref |
|---|---|---|---|
| MnO2 NPs (107 nm) loaded with poly(N-vinylcaprolactam) nanogels (PVCL NGs) (DOX/MnO2@PVCL NG). |
Treatment: DOX Cancer model: melanoma cancer model (B16 cancer cell line). In vivo: mouse model of subcutaneous B16 melanoma. |
NPs showed interesting biocompatibility properties in addition to redox responsiveness in tumoral tissues. In an in vivo tumor model (with relatively high concentration of GSH), a release of Mn+2 from DOX/MnO2@PVCL NG occurred that enhanced T1-weighted MRI. In parallel, the DOX release from the NPs inhibited the tumor growth (1 versus 14 relative tumor growth for dual-treatment and control, respectively). |
[103] |
| Fe3O4 IONPs (200–300 nm) were synthesized and functionalized with PDA, PEG, and cRGD (Fe3O4@PDA-PEG-cRGD). |
Treatment: DOX + photothermal effect (1 W/cm2). Cancer model: colon cancer model (HCT-116 cancer cell line). Male nude mice were subcutaneously injected with HCT-116 cells (5 × 106/mL). |
In vitro and in vivo, NPs were capable of targeting tumor cells and promoting the drug internalization. The cytotoxic effect was also significant (survival rate of 25.6% comparatively to control group) whilst the nanocarriers displayed good thermal stability and photothermal conversion efficiency, pH responsiveness, and an enhancement of T2-MRI contrast. In vivo, the authors observed a decrease in tumor growth around 67% when compared the dual-treatment with the control. | [104] |
| IONPs (26 nm) were coated with casein (CION) and functionalized with the tumor-targeting ATF of urokinase plasminogen activator and the antitumor drug CDDP (ATF-CNIO-CDDP). |
Treatment: CDDP. Cancer model: pancreatic cancer model (MIA PaCa-2 cancer cell line). Female nu/nu mice were injected with 1 × 106 MIA PaCa-2 cells (orthotopic pancreatic tumor model). |
NPs promote a T2-MRI contrast, combined with an improvement of therapeutic effectiveness (0.75 g versus 1.5 g of tumor weight for treated group and control, respectively) and a decrease on harmful side effects in comparison to the free drug. | [105] |
| SPIONs (260 nm) were coated with FA and ACPP (F/A-PLGA@DOX/SPIO). |
Treatment: DOX. Cancer model: human non-small cell lung cancer model (A549 cell line). Normal liver cell (L02 cell line). Male BALB/c nude mice were subcutaneously injected with 3 × 107 A549 cells into the right-rear leg. |
F/A-PLGA@DOX/SPIO induced apoptosis in the cancer cells, accelerating the overproduction of ROS. MRI was used to track the NPs in cancer cells (T2-weighted MRI). In vivo, a reduction in tumor growth was observed (around 67% comparatively to control group), NPs showed a good biocompatibility and long plasma stability, with a capability to induce tumor necrosis, whilst no significant damage or inflammation was detected in healthy organs. | [106] |
| SPIONs (6 nm) were coated with dextran (FeDC-E NPs). |
Treatment: erlotinib. Cancer model: lung cancer model (CL1-5-F4 cancer cell line). Male BALB/c nude mice were subcutaneously injected with 2.5 × 106 of CL1-5-F4 cells. |
Theranostic NPs showed a significant therapeutic effect with targeting properties against invasive and migrative cancer cells. These NPs enabled their localization using T2-weighted MRI. EGFR–ERK–NF-κB signaling pathways were suppressed when after tumors treatment. | [107] |
SPIONs: superparamagnetic iron oxide nanoparticles; IONPs: iron oxide nanoparticles; MNPs: magnetic nanoparticles; NPs: nanoparticles; DOX: doxorubicin; PDA: polydopamine; PEG: poly(ethylene glycol); cRGD: cyclic arginine-glycine-aspartate motif; ATF: amino-terminal fragment; GSH: glutathione; MRI: magnetic resonance imaging; CDDP: cisplatin; FA: folic acid; ACPP: activable cell-penetrating peptide; ROS: reactive oxygen species.