文献类型：期刊文献

中文题名：Chitopentaose inhibits hepatocellular carcinoma by inducing mitochondrial mediated apoptosis and suppressing protective autophagy

作者：Chunfeng Zhu[1];Mengyao Zhao[1,3];Liqiang Fan[1,3];Xuni Cao[1,3];Quanming Xia[1];Jiachun Zhou[1,3];Hao Yin[4];Liming Zhao[1,2,3]

机构：[1]School of Biotechnology,State Key Laboratory of Bioreactor Engineering,East China University of Science and Technology,No.130 Meilong Road,Shanghai,200237,China;[2]School of Life Sciences,Shandong University of Technology,Zibo,255049,China;[3]Shanghai Collaborative Innovation Center for Biomanufacturing Technology (SCICBT),Shanghai,200237,China;[4]Organ Transplant Center,Shanghai Changzheng Hospital,Shanghai,200003,China

年份：2021

卷号：8

期号：1

起止页码：1830

中文期刊名：Bioresources and Bioprocessing

外文期刊名：生物资源与生物加工(英文)

基金：supported by “Shu Guang” project of Shanghai Municipal Education Commission and Shanghai Education Development Foundation(15SG28);the China Postdoctoral Science Foundation(2017M621392);Fundamental Research Funds for the Central Universities(22221818014);the Open Project Funding of the State Key Laboratory of Bioreactor Engineering,ECUST(ZDXM2019);the Shanghai PuJiang Program(18PJ1401900).

语种：英文

中文关键词：Chitooligosaccharides;Singular DP;HCC;Apoptosis;Autophagy

摘要：Hepatocellular carcinoma (HCC) is one of the most prevalent and deadliest cancers.In this study,the anti-tumor effect of singular degree of polymerization (DP) chitooligosaccharides (COS) (DP 2-5) and the underlay molecular mechanisms were investigated on HCC cell line HepG2.MTT assay showed that (GlcN)5 have the best anti-proliferation effect among the different DP of COS (DP2-5).Furthermore,the administration of (GlcN)5 could decrease mitochondrial membrane potential,release cytochrome c into cytoplasm,activate the cleavage of Caspases9/3,thus inducing mitochondrial-mediated apoptosis in HepG2 cells (accounting for 24.57 ± 2.25%).In addition,(GlcN)5 treatment could increase the accumulation of autophagosomes.Further investigation showed that (GlcN)5 suppressed protective autophagy at the fusion of autophagosomes and lysosomes.Moreover,the inhibition of protective autophagy flux by (GlcN)5 could further decrease cell viability and increase the apoptosis rate.Our findings suggested that (GlcN)5 suppressed HepG2 proliferation through inducing apoptosis via the intrinsic pathway and impairing cell-protective autophagy.COS might have the potential to be an agent for lowering the risk of HCC.