Chitopentaose inhibits hepatocellular carcinoma by inducing mitochondrial mediated apoptosis and suppressing protective autophagy

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...

Full description

Bibliographic Details
Main Authors: Cao, X. (Author), Fan, L. (Author), Xia, Q. (Author), Yin, H. (Author), Zhao, L. (Author), Zhao, M. (Author), Zhou, J. (Author), Zhu, C. (Author)
Format: Article
Language:English
Published: Springer Science and Business Media Deutschland GmbH 2021
Subjects:
HCC
Online Access:View Fulltext in Publisher
LEADER 02205nam a2200277Ia 4500
001 10.1186-s40643-020-00358-y
008 220427s2021 CNT 000 0 und d
020 |a 21974365 (ISSN) 
245 1 0 |a Chitopentaose inhibits hepatocellular carcinoma by inducing mitochondrial mediated apoptosis and suppressing protective autophagy 
260 0 |b Springer Science and Business Media Deutschland GmbH  |c 2021 
856 |z View Fulltext in Publisher  |u https://doi.org/10.1186/s40643-020-00358-y 
520 3 |a 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.[Figure not available: see fulltext.] © 2021, The Author(s). 
650 0 4 |a Apoptosis 
650 0 4 |a Autophagy 
650 0 4 |a Chitooligosaccharides 
650 0 4 |a HCC 
650 0 4 |a Singular DP 
700 1 |a Cao, X.  |e author 
700 1 |a Fan, L.  |e author 
700 1 |a Xia, Q.  |e author 
700 1 |a Yin, H.  |e author 
700 1 |a Zhao, L.  |e author 
700 1 |a Zhao, M.  |e author 
700 1 |a Zhou, J.  |e author 
700 1 |a Zhu, C.  |e author 
773 |t Bioresources and Bioprocessing