Table 3

The theranostic applications of MNPs-based DDS in colorectal cancer treatment

NanoDDSPreparation methodTumor modelDiagnostic modeTherapeutic modeIn vivo efficacyReference
PTX-SPIO-PEALCa micellePolymer self-assemblyLoVo xenograft tumorMRIChemotherapyThe tumor volumes of PTX-SPIO-PEALCa, Taxol, and PBS groups at day 30 were 65.0 ± 8.4, 598.7 ± 77.4, and 1050.7 ± 54.4 mm3, respectively112
PTX-PFOB-(PLGA-PEG)Emulsion evaporationCT-26 xenograft tumorMRIChemotherapyTwo-fold reduction of tumor growth compared to control and Taxol® groups113
5-FU-magnetite-PLGAO/W/O/W multiple emulsion and solvent evaporationCT-26 allograft modelMRIChemotherapyThe nanocapsules showed more efficient tumor volume inhibition (100 mm3 at day 21) than 5-FU alone (1500 mm3)114
Cisplatin-magnetite-P(MAA-g-EGMA)Hydrolytic alkaline precipitationHT-29 xenograft tumorMRI
PET
CT
ChemotherapyThe tumor volumes of nano-assemblies+external magnetic field, nano-assemblies, and free cisplatin at day 38 were 300, 400, and 900 mm3, respectively115
Oxaliplatin-SPIO-MWNTs-PEGPolyol processHCT-116 tumor-bearing miceMRIChemotherapyNanotheranostics showed more effective tumor inhibition than oxaliplatin, with trivial weight loss (6.25%) and organ toxicity116
PTX-F127-SIONRHydrothermal methodCT-26 xenograft tumorMRIChemotherapyPTX-F127-SIONR exhibited higher therapeutic response and lower tumor growth than PTX group, which showed comparable tumor size to control group, and 100% death at day 34117
DOX-Fe3O4 MNPsCo-precipitationHT-29 cells in vitroMRIChemotherapyDOX-MNPs showed higher cytotoxicity (IC50 = 0.245 μmol/L) than free DOX (IC50 = 0.757 μmol/L)118
MANPs-PTXOne step oxidation methodCT-26 xenograft tumorMRIChemoradiation therapyMANPs-PTX inhibited tumor growth of 96.57%; other treatments showed insufficient efficacy119
Anti-MG1-HNPsHigh temperature hydrolysis reactionCC-531-implanted Wistar ratsMRIPTAThe tumor inhibition rates of anti-MG1-HNPs, HNPs, and control groups were 38% ± 29%, 14% ± 17%, and 7% ± 8%, respectively120
Aptamer-Au@SPIONsMicroemulsionHT-29 cells in vitroMRIPTT80% cell inhibition rate, at 500 µg/mL system concentration and 820 nm NIR exposure121
Au-HNPs-scFvSW1222 xenograft tumorMRIPTTThe tumor volumes of HNPs-scFv, laser only, non-targeted HNPs, and control groups were 72 ± 7, 161 ± 15, 195 ± 10, and 193 ± 18 mm3, respectively122
A33scFv-HNPsThermal decompositionSW1222 cellsHT-29 cells in vitroMRIPTTAfter 6 min treatment of 808 nm laser, > 53% of SW1222 cells were involved with apoptosis-related cell death while < 5% occurred in HT-29 cells123
Au@Gd2O3:Ln (Ln = Yb/Er)Seed-mediated growth methodCC-531 xenograft tumorMRIPTTUnder 808 nm NIR light irradiation for 5 min, the tumor temperature increased by ~19.5 °C in the NPs group, showing a stronger PTT effect than the control (~7.5 °C)124
HANsThermal decompositionHT-29 xenograft tumorMRI
PAI
Chemotherapy
PTT
The tumor volume of the HANs+laser group remained ~0 without a relapse, which was reduced slightly in the HANs alone group, while the tumor grew rapidly after laser treatment without the HANs and PBS groups125
MGO-PEG-CETCo-precipitationCT-26 BALB/c miceMRIChemotherapy
PTT
The relative tumor volumes of control, DOX, MGO-PEG-CET/DOX, MGO-PEG-CET/DOX+magnet, and MGO-PEG-CET/DOX+magnet+laser were 12.1, 10.1, 9.5, 5.8, and 0.42, respectively126
Fe-CPNDsCoordination reactionSW620 xenograft tumorMRIPTTComplete tumor ablation at day 20127
Hypericin-SPIONsCo-precipitationHT-29 cells in vitroMRIPDTCell proliferation was completely abolished at 2 µmol/L of hypericin and 60 h of illumination time128
SiRNA plasmid-AuLoVo bearing nude miceMRIGene therapyBag-1 protein level was silenced to 60% of control, and caused the debasement of Wnt pathway129
SN-38/USPIO-siRNA-PEGO/W emulsion and solvent evaporationLS174T bearing nude miceMRIChemotherapy
Gene therapy
The tumor volumes of SN-38/USPIO/siRNA, SN-38/USPIO, and SN-38 groups were 340 ± 52, 591 ± 125, and 1,150 ± 362 mm3, respectively130

SPIO, superparamagnetic iron oxide; SIONR, SPIO nanorods; USPIO, ultra-small SPIO; Fe3O4, iron-oxide; PFOB, perfluorooctyl bromide; MWNTs, multiwalled carbon nanotubes; MNPs, magnetic nanoparticles; MnO2, manganese dioxide; HNPs, hybrid magnetic gold nanoparticles; HANs, hybrid anisotropic nanoparticles; CPNDs, coordination polymer nanodots; Au, gold; Gd, gadolinium; Ln, lanthanide; Yb, ytterbium; Er, erbium; MGO, magnetic graphene oxide; PEALCa, PEG-P(Asp-DIP)-P(Lys-Ca); PEG, polyethylene glycol; P(Asp-DIP), poly(N-(N′,N′-diisopropylaminoethyl) aspartamide); P(Lys-Ca), poly (lysine-cholic acid); PLGA, poly(lactide-co-glycolide); P(MAA-g-EGMA), poly(methacrylic acid)-g-poly(ethyleneglycol methacrylate); F127, pluronic F127; MANPs, MnO2 functioned albumin nanoparticles (ANPs); PTX, paclitaxel; 5-FU, 5-fluorouracil; DOX, doxorubicin; SN-38, 7-ethyl-10-hydroxycamptothecin; PBS, phosphate-buffered saline; O, oil; W, water; IC50, half maximal inhibitory concentration; MG1 mAbs, a monoclonal antibody localized to rat colorectal liver metastasis cells; scFv, single-chain variable fragment; A33, an antigen presented on some CRC cells such as SW1222; CET, cetuximab, an EGFR monoclonal antibody; siRNA, small interfering RNA; Bag-1, Bcl-2-associated athanogene 1; MRI, magnetic resonance imaging; PET, positron emission tomography; CT, computed tomography; PAI, photoacoustic imaging; PTA, photothermal ablation; PTT, photothermal therapy; PDT, photodynamic therapy; NIR, near infrared; CRC, colorectal cancer, LoVo cells, human CRC cells; CT-26 cells, murine colon cancer cells; HT-29 cells, human colon cancer cells; HCT-116 cells, human colon cancer cells; CC-531 cells, rat colorectal liver metastasis cells; SW1222 cells, human CRC cells; SW620 cells, human CRC cells; LS174T cells, human colon cancer cells; DDS.