No abstract

Background: Gold nanoshells can be tuned to absorb a particular wavelength of light. As a result, these tunable nanoparticles (NPs) can efficiently absorb light and convert it to heat. This phenomenon can be used for cancer treatment known as photothermal therapy. In this study, we synthesized Fe3O4@Au core-shell NPs, magnetically targeted them towards tumor, and used them for photothermal therapy of cancer.Objective: The main purpose of this research was to synthesize Fe3O4@Au core-shell NPs, magnetically target them towards tumor, and use them for photothermal therapy of cancer.Material and Methods: Twenty mice received 2 × 106 B16-F10 melanoma cells subcutaneously. After tumors volume reached 100 mm3,the mice were divided into five groups including a control group, NPs group, laser irradiation group, NPs + laser group and NPs + magnet + laser group. NPs were injected intravenously. After 6 hours, the tumor region was irradiated by laser (808 nm, 2.5 W/cm2, 6 minutes). The tumor volumes were measured every other day.Results: The effective diameter of Fe3O4@Au NPs was approximately 37.8 nm. The average tumor volume in control group, NPs group, laser irradiation group, NPs + laser irradiation group and NPs + magnet + laser irradiation group increased to 47.3, 45.3, 32.8, 19.9 and 7.7 times, respectively in 2 weeks. No obvious change in the average body weight for different groups occurred.Conclusion: Results demonstrated that magnetically targeted nano-photothermal therapy of cancer described in this paper holds great promise for the selective destruction of tumors.

No abstract

AIM: Tamoxifen engages mitochondrial estrogen receptor beta as an antagonist, increases mitochondrial cytotoxicity and induces tumor cell death. Tamoxifen also engages plasma membrane estrogen receptor alpha as an agonist, while it is suggested that in some users its activation is put into action by mechanism of resistance to tamoxifen. Apoptotic inducers have been shown to promote tamoxifen-induced cell death, which might be of great importance in overcoming tamoxifen resistance. Considering the pleiotropic effects of statins, in the present study, we investigated the effects of atorvastatin on tamoxifen-induced intrinsic apoptotic pathway activity in melanoma cells. METHODS: Melanoma B16F10 cells were treated for 24 and 48 h with various concentrations of tamoxifen, atorvastatin and combination of tamoxifen + atorvastatin. Cells with no treatment were considered a control group, and the study was then followed by quantitative RT-PCR assay. Bax and cytochrome c gene expressions were calculated by ΔΔct method. RESULTS: Co-treatment of atorvastatin + tamoxifen could strongly enhance the expression of pro/apoptotic factors of Bax and cytochrome c in melanoma cells compared to the tamoxifen and atorvastatin groups. CONCLUSION: In general, we conclude that the atorvastatin-induced increase in Bax and cytochrome c gene expression might be a permissive response to tamoxifen-induced cell death (Fig. 2, Ref. 37).

No abstract