Zinc ferrite magnetic nanomaterials induce reactive oxygen species and pro-death autophagy to kill renal cancer cells

Acta Universitatis Medicinalis Anhui 2021 08 v.56 1190-1196     font:big middle small

Found programs:

Authors:Yang Heyu; Zhang Li; Wen Huiqin

Keywords:renal cancer;zinc ferrite magnetic nanoparticles;ROS;autophagy

DOI:10.19405/j.cnki.issn1000-1492.2021.08.004

〔Abstract〕 Objective To investigate the killing effect of zinc magnetic ferrite nanomaterials(ZF NPs) on kidney cancer Caki-1 cells and its correlation with ROS and autophagy. Methods ZF NPs were synthesized by aqueous method and characterized by TEM and other methods. The inhibitory effect of ZF NPs on Caki-1 cells was detected by Thiazole Blue(MTT) assay. Intracellular ROS levels were detected by DCFH-DA staining. TEM was used to observe the autophagosomes in Caki-1 cells after ZF NPs treatment. The changes of autophagy effect were detected by Western blot. DCFH-DA staining, MTT and Western blot were used to investigate the regulation mechanism of ROS and autophagy induced by ZF NPs during the killing of CaKi-1 cells. Results ZF NPs with uniform size and shape were synthesized by aqueous method, which exerted paramagnetic properties for MRI. ZF NPs had a dose and time dependent killing effect on Caki-1 cells. In this process, ZF NPs could induce Caki-1 cells to produce dose and time dependent ROS, while NAC could reduce the production of ROS and weaken the killing effect of ZF NPs. ZF NPs could also elicit autophagy in Caki-1 cells. After co-treatment with Wortmannin, the accumulation of LC3-Ⅱ decreased and the subsequent cell viability was higher than that of ZF NPs treated alone, while co-treatment with Trehalose could increase ROS production and autophagic intensity in executing tumoricidal effect of ZF NPs. Among the sensitization process, NAC could reduce the accumulation of LC3-Ⅱ and Wortmannin could decrease ROS generation. Conclusion ZF NPs have the potential to become a MRI contrast agent, and can induce ROS and pro-death autophagy to kill Caki-1 cells.