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Chalcomoracin is a potent anticancer agent acting through triggering Oxidative stress via a mitophagy- and paraptosis-dependent mechanism

Scientific reports, 2018-06, Vol.8 (1), p.9566-14, Article 9566 [Peer Reviewed Journal]

2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2018 ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/s41598-018-27724-3 ;PMID: 29934599

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  • Title:
    Chalcomoracin is a potent anticancer agent acting through triggering Oxidative stress via a mitophagy- and paraptosis-dependent mechanism
  • Author: Han, Haote ; Chou, Chih-Chien ; Li, Ruyi ; Liu, Jiangyun ; Zhang, Lin ; Zhu, Wei ; Hu, Jin ; Yang, Bingxian ; Tian, Jingkui
  • Subjects: Acetylcysteine ; Antioxidants ; Antitumor agents ; Apoptosis ; Cancer ; Ectopic expression ; Endoplasmic reticulum ; Fungi ; Kinases ; Metabolites ; Morus ; Myc protein ; Oxidative stress ; PTEN protein ; PTEN-induced putative kinase ; Reactive oxygen species ; Secondary metabolites ; Xenografts
  • Is Part Of: Scientific reports, 2018-06, Vol.8 (1), p.9566-14, Article 9566
  • Description: Chalocomoracin (CMR), one of the major secondary metabolites found in fungus-infected mulberry leaves, is a potent anticancer agent. However, its anticancer mechanism remains elusive. Here, we demonstrated the potent anti-tumor activity and molecular mechanism of CMR both in vitro and in vivo. We showed for the first time that CMR treatment markedly promoted paraptosis along with extensive cytoplasmic vacuolation derived from the endoplasmic reticulum, rather than apoptosis, in PC-3 and MDA-MB-231cell lines. Additional studies revealed that ectopic expression of Myc-PINK1 (PTEN-induced kinase 1), a key regulator of mitophagy, rendered LNCap cells susceptible to CMR-induced paraptosis, suggesting that the mitophagy-dependent pathway plays a crucial role in inducing paraptosis by activating PINK1. CMR treatment directly upregulated PINK1 and downregulated Alix genes in MDA-MB-231 and PC-3 cell lines. Furthermore, mitophagy signaling and paraptosis with cytoplasmic vacuolation could be blocked by antioxidant N-acetylcysteine (NAC), indicating the novel pathway was triggered by reactive oxygen species (ROS) production. An in vivo MDA-MB-231 xenograft tumor model revealed that CMR suppressed tumor growth by inducing vacuolation production through the same signal changes as those observed in vitro. These data suggest that CMR is a potential therapeutic entity for cancer treatment through a non-apoptotic pathway.
  • Publisher: England: Nature Publishing Group
  • Language: English
  • Identifier: ISSN: 2045-2322
    EISSN: 2045-2322
    DOI: 10.1038/s41598-018-27724-3
    PMID: 29934599
  • Source: ProQuest Databases
    PubMed Central
    DOAJ Directory of Open Access Journals
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