Ultrasmall iron oxide nanoparticles induced ferroptosis via Beclin1/ATG5-dependent autophagy pathway

Wen Jian; Chen Hanren; Ren Zhongyu; Zhang Peng; Chen Jianjiao; Jiang Shulian

doi:10.1186/s40580-021-00260-z

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자료유형: 학술저널

저자정보: Wen Jian (Guilin Medical University) Chen Hanren (Guilin Medical University) Ren Zhongyu (Guilin Medical University) Zhang Peng (Guilin Medical University) Chen Jianjiao (Guilin Medical University) Jiang Shulian (Nanjing Second Hospital)

저널정보: 나노기술연구협의회 Nano Convergence Nano Convergence Vol.8 No.10

발행연도: 2021.4

수록면: 1 - 15 (15page)

DOI: 10.1186/s40580-021-00260-z

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Iron-based nanoparticles, which could elicit ferroptosis, is becoming a promising new way to inhibit tumor cell growth. Notably, ultrasmall iron oxide nanoparticles (USIONPs) have been found to upregulate the autophagy process in glioblastoma (GBM) cells. Whether USIONPs could also elicit ferroptosis and the relationship between the USIONPs-induced autophagy and ferroptosis need to be explored. In the current study, our synthesized USIONPs with good water solubility could significantly upregulate the ferroptosis markers in GBM cells, and downregulate the expression of anti-ferroptosis genes. Interestingly,ferrostatin-1 could reverse USIONPs- induced ferroptosis, but inhibitors of apoptosis, pyroptosis, or necrosis could not. Meanwhile, autophagy inhibitor 3-methyladenine could also reverse the USIONPs-induced ferroptosis. In addition, shRNA silencing of upstream genes Beclin1/ATG5 of autophagy process could significantly reverse USIONPs-induced ferroptosis, whereas overexpression of Beclin1/ATG5 of autophagy process could remarkably promote USIONPs-induced ferroptosis. Furthermore, lysosome inhibitors could significantly reverse the USIONPs-induced ferroptosis. Collectively, these facts suggest that USIONPs-induced ferroptosis is regulated via Beclin1/ATG5-dependent autophagy pathway.

#Autophagy Ferroptosis Ultrasmall iron oxide nanoparticle Autolysosome

참고문헌 (36)

참고문헌 신청

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