| | Tumor entity | Particle type | Main finding | Ref. |
| | Preclinical studies | | Lung cancer | Polyurethane NPs, superparamagnetic iron oxide NPs coated with silica layers, mesoporous silica NPs, zinc oxide NPs, triphenylphosphonium-Pluronic F127 nanomicelles, cetuximab chitosan NPs, polymeric NPs, polyethyleneimine NPs coated with bovine serum albumin | Reduction in cancer cell survival, apoptosis induction (upregulating caspase-3, caspase-9, PARP, Bax), inhibition of lung tumor growth, pausing growth of cancerous cells, decrease in tumor size, induction of DNA leakage from nuclei by ROS/RNS, inhibition of metastasis, cell cycle arrest at G2/M phase, prevention of autophagy | [180–187] |
| | Breast cancer | Porous silicon NPs, mesoporous maghemite NPs, PCE NPs, metal-organic frameworks, polymeric NPs (NVA-AA), porphyrin-based metal-organic framework carrier | Inhibition of metastasis; prevention of tumor growth; decrement of cell viability; suppression of cancer cell proliferation; reduction in tumor size; decrease in side effects; induction of apoptosis (downregulating Bcl-2 and upregulating caspase-3, UBA52, TIAL1, and PPP1C); suppression of cell motility and invasiveness; downregulating proteins involved in vesicular trafficking | [188–193] |
| | Ovarian cancer | Selenium NPs, poly (lactic-co-glycolic) acid NPs with inorganic molybdenum octahedral cluster, Fe2O3 NPs, PEGL NPs, chitosan copolymer-magnetic NPs, poly-ε-caprolactone NPs | Inhibition of cancer cell growth, cytotoxic effect on cancer cells, reduction of metastasis, decrease of cancer cell viability and cytotoxicity, increased the intracellular ROS/RNS, diminution of tumor volume | [194–199] |
| | Colon cancer | Albumin NPs, chitosan NPs, perfluorooctylbromide- porphyrin grafted lipid NPs, biosynthesized silver NPs, superparamagnetic iron oxide coated with mesenchymal stem cell, silver and gold NPs, mesoporous silica NPs coated with folic acid chitosan-glycine complex, hydroxyapatite NPs coated with gum Arabic, PLGA NPs co-loaded with 5-fluorouracil and perfluorocarbon | Enhancement of cancer cells killing; improved antitumor efficacy; prevention of tumor growth and metastasis; decrement of tumor volume; enhancement of photodynamic effects against cancer cells (by increasing oxidative stress); induction of apoptosis (overexpression of caspase-3, caspase-9, bid, and Bax); reduction of immune system response and systemic side effects; fragmentation of DNA in cancer cells; increase in antimitotic effects | [200–207] |
| | Glioblastoma | Silver NPs, lanthanum oxide NPs, transferrin-conjugated porous silicon NPs, high-Z metal NPs, PEI surface-functionalized mesoporous silica NPs, PLGA NPs coated with polyvinyl alcohol and Poloxamer188, magnetic iron oxide NPs loaded trimethoxysilylpropyl-ethylenediamine triacetic acid, polymerized human serum albumin NPs, PEI-PEG-magnetic iron oxide NPs | Immense antitumor effect, increase in caspase activity, increase intrinsic and extrinsic apoptosis, diminution tumor cell viability, induce DNA damage and autophagic pathways, enhancing ROS/RNS, pausing cancer cell migration, causing a rupture of the lysosomal membranes, inhibition of cancer cell proliferation, downregulation of crucial enzymes for DNA repair and replication in cancer cells, upregulation of tumor suppressors | [208–214] |
| | Pancreatic cancer | Magnetic NPs, nitric oxide donor S-nitroso-N-acetylpenicillamine loaded liposomes, PLGA NPs, polyanhydride NPs, solid lipid NPs, porous coordination network-Fe (III) NPs | Tumor growth inhibition, efficient tumor retention, enhancement of cytotoxicity; decrease of cell proliferation, reduction in cancer metastasis and progression, overexpression of proapoptotic genes, induction of ROS/RNS, improvement of anticancer treatment efficacy | [215–220] |
| | Bone cancer | Superparamagnetic γ-Fe2O3 iron oxide with SiO2-CaO shell NPs, zinc oxide NPs; Fe ions-releasing mesoporous NPs, NPs with magnetic inner core and polymeric outer shell, alendronate-poly(amidoamine) NPs, metal-organic framework NPs | Increase of cytotoxicity in cancer cells, suppression of cancer cell growth, induction of apoptosis, exhibition of anticancer action, inhibition of the formation of osteoclasts, prevention of metastasis, induction of the polarization of tumor-resident macrophages to M1 phenotype | [221–226] |
| | Prostate cancer | Selenium NPs, PLGA-PEG NPs, superparamagnetic iron oxide NPs, human serum albumin-coated NPs of (2) Ga, lipid-polymer hybrid NPs, manganese oxide–mesoporous silica, hexagonal boron nitride NPs | High anticancer activity, induction of tumor cell death via necrosis, increase of cytotoxicity, tumor regression, cell death induction, disruption of lysosomal structure in cancer cells, attenuation of lysosomal protease activity, modulator of autophagy | [227–232] | | Liver cancer | Fe3O4-au nanoheterostructures, hydroxycamptothecin-based polyprodrug as the inner core, amphiphilic lipid-PEG as the outer shell NPs, exonanoRNA NPs, chondroitin-modified lipid NPs, glycogen NPs, rubber-like RNA NPs, CoFe2O4@MnFe2O4 magnetic NPs, mesoporous silica NPs | Significant cytotoxicity in cancerous cells, inhibition of tumor growth, induction of apoptosis, reduction in cell proliferation, increase of antitumor efficacy, inducing the enhanced permeability and retention effect, increment the release rate of the drug, reducing systemic side effects | [233–239] |
| | Clinical trials | | Solid tumor in advanced stage | CYT-6091 (consist of AuNPs-PEG and tumor necrosis factor-α) | Treatment was well-tolerated, and one partial response was observed among 29 patients in this phase I study | [240, 241] |
| | Colorectal cancer | CPX-1 (liposome-encapsulated formulation of irinotecan and floxuridine) | 11 out of 13 patients showed disease control while 2 patients showed partial response | [242] |
| | Breast cancer, lung cancer, colorectal cancer | FCE28068 (anthracycline doxorubicin linked to copolymers based on N-(2-hydroxypropyl) methacrylamide) | Response in breast and lung cancer patients, no response in colorectal cancer patients | [243] |
| | Stomach cancer | MCC-465 (PEG immunoliposome-encapsulated doxorubicin) | Acute reactions related to infusion observed, no antitumor response observed, stable disease (SD) observed in 10 of 18 patients | [244] |
| | Adenocarcinoma of the esophagus and gastroesophageal junction | SP1049C (doxorubicin in P-glycoprotein-targeting Pluronic) | 9 out of 21 patients showed partial response, and 8 patients had either a minor response or stable disease | [245] |
| | Advanced pancreatic cancer | Rexin-G (retroviral vector expressing a cytocidal cyclin G1 construct) | No antitumor activity observed | [246] |
| | Pancreatic cancer | NK105 (a paclitaxel-incorporating micellar nanoparticle) | Partial response observed in 1 out of 11 patients, significant myelosuppression not observed up to 80 mg/m−2, pain or local toxicity in the area of the injection not observed in any patient, and 10 patients did not experience any hypersensitivity during the study | [247] |
| | Pancreatic cancer | Lipoplatin (liposomal cisplatin) and gemcitabine | Partial response in 2/24 patients, disease stability in 14 patients, clinical benefit in 8 patients | [248] |
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