Table 4.

Solid lipid nanoparticles (SLNs) as drug delivery systems for cancer therapy.

SLN (Particle Size) + Surface Modification/Loading	Drug + Cancer Model	Results	Ref
SLNs (200 nm). Surface modification is not mentioned.	Drug: DOX. Cancer model: murine malignant melanoma (B16F10 cells). C57BL/6 mice (12–16 weeks old) were intravenously injected with 1 × 105 B16F10 cells.	In vivo, mice treated with SLNs-DOX, obtained, approximately, a 60% reduction of tumor area when compared to mice treated with free DOX. No significant differences were found in the survival rates or body weight between different treatment groups, indicating no detectable SLPs-DOX in vivo toxicity during the timeframe of these tests.	[151]
PTX-SLN (<200 nm). Surface modification is not mentioned.	Drug: PTX. Cancer model: breast cancer model (MCF-7 cancer cell line).	Xu et al. observed an enhanced anticancer activity of PTX-SLNs, which significantly increased the intracellular uptake (almost 10 ng more of PTX per mg of protein comparatively to control) of the drug when compared to the free drug. The results demonstrated that the use of SLNs could efficiently avoid the multidrug resistance mechanisms observed in breast cancer cells.	[147]
SLN-TMZ (279 nm). Surface modification is not mentioned.	Drug: TMZ. Cancer model: melanoma cancer model (JR8 and A2058 cell lines; B16-F10 mouse melanoma cell line). Female C57BL6/J mice were subcutaneously injected with 1 × 106 B16-F10 cells.	NPs showed in vitro and in vivo their ability to target tumor cells and promote drug internalization, reducing the therapeutic dosage needed to be administered in the in vivo model. Here, SLN-TMZ also displayed a higher mice survival rate compared to that obtained using the free drug (increasing from 50 to 100%). Moreover, the in vitro tumor angiogenesis was found to be inhibited (HUVEC method).	[152]
Chol-CUR-SLN (170 nm). Surface modification is not mentioned.	Drug: CUR. Cancer model: breast cancer model (MDA-MB-231 cell line).	In vitro results showed that Chol-CUR-SLN efficiently targeted and accumulated in cancer cells. It also exhibited a higher inhibitory effect on cell viability (20% of higher cytotoxicity in comparison to free drug) and proliferation when compared to free CUR. Chol-CUR-SLN significantly improved the induction of apoptosis (63.87% versus 55.4%) in MDA-MB-231 cells, compared to free CUR.	[153]
SLN-MTX (300 nm) loaded with an ApoE mimicking chimera peptide to actively target the brain.	Drug: MTX. Cancer model: glioblastoma cancer model (F98/Fischer glioblastoma human primary culture).	A reduction of tumor growth (relative tumor growth of approximately 4 versus 10 for treated and control groups, respectively) was observed with SLN-MTX. Moreover, an increase of apoptosis was noted, demonstrating that the developed SLN could be an alternative to conventional therapy.	[154]
TAT PTX/TOS-CDDP SLNs (100 nm) modified with DSPE-PEG and TAT for co-delivery of PTX and TOS-CDDP.	Drug: PTX + TOS-CDDP. Cancer model: cervical cancer model (HeLa cancer cell line). BALB/c nude mice were subcutaneously injected with 1 × 106 of HeLa cells.	TAT PTX/TOS-CDDP SLNs had a slower drug release in comparison with PTX/TOS-CDDP SLNs. Here, the drug release was greatly affected by a lower pH. The in vitro cellular uptake study also showed that tumor cells could uptake more efficiently the TAT PTX/TOS-CDDP SLNs when compared with other SLNs. Moreover, these nanoparticles showed a synergistic effect in the suppression of tumor growth in vivo (inhibition rate of 72.2%) with lower toxicity (calculated by the bodyweight loss during the experiment). Moreover, the formulation increased the drug accumulation in tumor tissue in comparison to the administration of the free drug.	[155]
c-SLN (200 nm). Surface modification is not mentioned.	Drug: FA+ ASP. Cancer model: pancreatic cancer model (PaCa-2 and Panc-1 cell lines). Male SCID mice were subcutaneously injected with 1 × 106 PaCa-2 cells.	In vitro studies demonstrated that NPs with the conjugated treatment effectively inhibited cell growth, inducing apoptosis. The use of the dual treatment loaded in the SLNs presented significantly better results in cell viability assays when compared to the cells treated with the free drugs. The in vivo studies presented a tumor growth suppression of 45% compared to the control group. However, this result was not statistically significant. By performing the immunohistochemistry analysis, an increased expression of pro-apoptotic proteins was detected.	[156]

SLNs: solid lipid nanoparticles; NPs: nanoparticles; PTX: paclitaxel; TMZ: temozolomide; CUR: curcumin; Chol: cholesterol; ApoE: very low-density lipoprotein receptor binding; MTX: methotrexate; DSPE: 1,2-distearoyl-sn-glycero-3-phosphorylethanolamine; PEG: poly(ethylene glycol); TAT: trans-activating transcriptional activator; TOS-CDDP: α-tocopherol succinate-cisplatin prodrug; c-SLN: chitosan-coated solid lipid nanoparticle; FA: ferulic acid; ASP: aspirin; DOX: doxorubicin; HUVEC: human umbilical vein endothelial cells.