Nanosize aminated fullerene for autophagic flux activation and G0/G1 phase arrest in cancer cells via post-transcriptional regulation  

作　　者：Xiaoyan Zhang Wei Zhou Yang Liu Linyu Jin Jiawei Huo Yang Yang Shumu Li Haijun Ma Jiao Li Mingming Zhen Jie Li Chunru Wang 

机构地区：[1]Beijing National Research Center for Molecular Sciences,Key Laboratory of Molecular Nanostructure and Nanotechnology,Institute of Chemistry,Chinese Academy of Science,Beijing 100190,China [2]Department of Spinal Surgery,Peking University People’s Hospital,Peking University,Beijing 100034,China

出　　处：《Nano Research》2022年第4期3346-3355,共10页纳米研究（英文版）

基　　金：This work was supported by the National Natural Science Foundation of China(No.51802310);All animal experiments were conducted according to protocols approved by the Institutional Animal Care and Use Committee in the Institute of Chemistry,Chinese Academy of Sciences.

摘　　要：Functional fullerene derivatives exhibit special inhibitory effects on tumor progress and metastasis via diverse tumor microenvironment regulations,while the elusive molecular mechanisms hinder their clinical transformation.Herein,it is initially revealed that nanosize aminated fullerene(C_(70)-EDA)can activate autophagic flux,induce G0/G1 cell cycle arrest to abrogate cancer cell proliferation,and significantly inhibit tumor growth in vivo.Mechanismly,C_(70)-EDA promotes the expression of cathepsin D involved in autophagic activation via post-transcriptional regulation,attributing to the interaction with a panel of RNA binding proteins.The accumulation of cathepsin D induces the autophagic degradation of cyclin D1,which arouses G0/G1 phase arrest.This work unveils the fantastic anti-tumor activity of aminated fullerene,elucidates the molecular mechanism,and provides a new strategy for the antineoplastic drug development on functional fullerenes.

关 键 词：aminated fullerene autophagic flux G0/G1 phase arrest post-transcription regulation 

分 类 号：R73[医药卫生—肿瘤]