TABLE 3.
A summary of CS‐based nanostructures for DOX delivery in cancer suppression
| Nanostructure | Particle size (nm); zeta potential (mV); encapsulation efficiency or drug loading (%) | Cancer type | In vitro/in vivo | Cell line/animal model | Remarks | Referencs |
|---|---|---|---|---|---|---|
| Estrogen‐functionalized CS nanoparticles | 198.2 and 206.4 nm; 28.3 and 30.6 mV; up to 66.33% | Breast cancer | In vitro | MCF‐7 cells | High biocompatibility and antineoplastic activity | 278 |
| CS‐raloxifene nanoparticles | 26.85 and 34.75 nm; 0.17 and −0.49 mV; up to 98% | Breast cancer | In vitro | MCF‐7 cells |
Decreasing proliferation rate by 60% Nanoparticles inhibit cancer progression via suppressing estrogen receptor |
279 |
| DOX‐loaded LGCC NPs | 200 nm; 20–35 mV; up to 86.4% | Breast and liver cancers | In vitro; in vivo |
QGY‐7703 and 4 T1 cells H22 hepatocarcinoma model |
Penetrating directly via cell membrane and circumventing endocytic vesicles Cargo release under high GSH levels Endosomal and lysosomal escape High nuclear distribution |
262 |
| Catechol‐modified CS‐hyaluronic acid nanoparticles | 160 nm; −19.8 mV | Oral cancer | In vitro | HN22 cells |
Negative charge and spherical shape High mucoadhesive ability Prolonged release of DOX Reducing cancer proliferation |
280 |
| Ethyl cellulose/CS/g‐C3N4/MoS2 core–shell nanofibers | 285–370 nm | Breast and cervical cancers | In vitro | MCF‐7 and HeLa cells |
Sustained delivery of DOX Inducing cell death up to 89% and 85% in MCF‐7 and HeLa cells, respectively in 7 days |
281 |
| Aptamer‐functionalized CS‐bases silica nanostructures | 87 nm; 35.9 to −32.3 mV | Breast cancer | In vitro; in vivo |
MCF‐7 and 4 T1 cells C26 tumor‐bearing mice |
Enhanced cellular uptake Targeted delivery of DOX and anti‐miRNA‐21 in cancer suppression |
282 |
| PEGylated CS nanoparticles | 169–192 nm; up to 43 mV | Breast cancer | In vitro | MCF‐7 cells |
Functionalization of CS nanoparticles with anti‐hMAM and anti‐HER2 promotes selectivity toward cancer cells Exerting dose‐dependent toxicity against cancer cells |
283 |
| CMC/PCL nanofibers | 300 nm; higher than −30 mV; 90% | Breast cancer | In vitro | MCF‐7 cells |
Lack of initial burst release Sustained release for 7 and 25 days Cytotoxicity against tumor cells up to 85% |
284 |
| HMSN grafted with CS‐copper sulfide composites | 150 nm; −19.6 mV; 46.1% | Breast cancer | In vitro; in vivo |
MDA‐MB‐231 cells Mouse model of breast cancer |
High biocompatibility Increased cellular uptake by cancer cells Apoptosis induction Increasing survival of mice |
285 |
| CS‐, PEG‐ and PVA‐modified MgFe2O4 ferrite magnetic nanoparticles | 78–140 nm; below −21 mV | Breast and colorectal cancers | In vitro | Caco‐2 and SKBR‐3 cells |
Decreasing cancer cell viability in a concentration‐dependent manner pH‐sensitive release of DOX 85.86% release of DOX after 72 h |
286 |
| CS hydrogel beads | 13.5 mV | Breast cancer | In vitro | MCF‐7 cells |
High swelling rate (426%) and drug release (81.33% in 144 h) at pH of 5.8 High biocompatibility Decreasing proliferation rate of MCF‐7 cells |
287 |
| CMCS/MAGG hydrogel | ‐ | Breast cancer | In vitro | MCF‐7 cells |
pH‐responsive swelling of hydrogels 67.06% release of DOX after 5 days in pH of 5.5 32.13% release of DOX at pH of 7.4 High biocompatibility Cytotoxicity against MCF‐7 cells |
287 |
Abbreviations: CMC, N‐carboxymethyl chitosan; CS, chitosan; DOX, doxorubicin; GSH, glutathione; HMSN, hollow mesoporous silica nanoparticle; NPs, nanoparticles; PCL, poly(ε‐caprolactone); PVA, polyvinyl alcohol, PEG, polyethylene glycol.