文献类型：期刊文献

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

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

机构：[1]East China Univ Sci & Technol, Sch Biotechnol, State Key Lab Bioreactor Engn, 130 Meilong Rd, Shanghai 200237, Peoples R China;[2]Shandong Univ Technol, Sch Life Sci, Zibo 255049, Peoples R China;[3]Shanghai Collaborat Innovat Ctr Biomfg Technol SC, Shanghai 200237, Peoples R China;[4]Shanghai Changzheng Hosp, Organ Transplant Ctr, Shanghai 200003, Peoples R China

年份：2021

卷号：8

期号：1

外文期刊名：BIORESOURCES AND BIOPROCESSING

收录：;EI(收录号：20224513084344);WOS:【SCI-EXPANDED(收录号:WOS:000605207600001)】；

基金：This work was 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), and the Shanghai PuJiang Program (18PJ1401900).

语种：英文

外文关键词：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.