α -Hederin Arrests Cell Cycle at G2/M Checkpoint and Promotes Mitochondrial Apoptosis by Blocking Nuclear Factor-κB Signaling in Colon Cancer Cells.

Colon cancer represents the third most common malignancy worldwide. New drugs with high efficaciousness and safety for the treatment of colon cancer are urgently needed in clinical context. Here, we were aimed to evaluate the antitumor activity of the natural compound α-hederin in human colon cancer...

Descripción completa

Detalles Bibliográficos
Publicado en:BioMed Research International Vol. 2018; pp. 1 - 12
Autores principales: Sun, Dongdong, Shen, Weixing, Zhang, Feng, Fan, Huisen, Tan, Jiani, Li, Liu, Xu, Changliang, Zhang, Haibin, Yang, Ye, Cheng, Haibo
Formato: pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell 9/27/2018
Acceso en línea:Ver este registro en EBSCOhost
fields @attributes:
  recordID: 1
pdfLink:
plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=132009683&site=ehost-live
header:
  @attributes:
    shortDbName: ccm
    uiTerm: 132009683
    longDbName: CINAHL Complete
    uiTag: AN
  controlInfo:
    bkinfo:
    dissinfo:
    jinfo:
      jid:
        23146133
        FT2T
      jtl: BioMed Research International
      issn: 23146133
      maglogo: N
    pubinfo:
      dt: 9/27/2018
      vid: 2018
      pid: 480
      pub: Wiley-Blackwell
      place: Malden, Massachusetts
    artinfo:
      ui:
        132009683
        132009683
        132009683
        10.1155/2018/2548378
        132009683
      ppf: 1
      ppct: 11
      formats:
        fmt:
          – @attributes:
              type: T
          – @attributes:
              type: P
      tig:
        atl: α -Hederin Arrests Cell Cycle at G2/M Checkpoint and Promotes Mitochondrial Apoptosis by Blocking Nuclear Factor-κB Signaling in Colon Cancer Cells.
      aug:
        au:
          Sun, Dongdong
          Shen, Weixing
          Zhang, Feng
          Fan, Huisen
          Tan, Jiani
          Li, Liu
          Xu, Changliang
          Zhang, Haibin
          Yang, Ye
          Cheng, Haibo
        affil: The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing 210023, China
      sug:
        subj:
          Steroids Pharmacodynamics
          Cell Cycle Drug Effects
          Mitochondria Drug Effects
          Apoptosis Drug Effects
          NF-kappa B Drug Effects
          Signal Transduction Drug Effects
          Colonic Neoplasms Drug Therapy
          Cell Line, Tumor Drug Effects
          Human
          Interleukins Drug Effects
          In Vitro Studies
          Inflammation
          Cell Viability Drug Effects
          RNA, Messenger Drug Effects
          Gene Expression Drug Effects
          Growth Substances Drug Effects
          Biochemical Phenomena Drug Effects
          Hemeproteins Drug Effects
          Caspases Drug Effects
          Transferases Drug Effects
          Biological Transport Drug Effects
          Phosphorylation Drug Effects
          Chelating Agents
      ab: Colon cancer represents the third most common malignancy worldwide. New drugs with high efficaciousness and safety for the treatment of colon cancer are urgently needed in clinical context. Here, we were aimed to evaluate the antitumor activity of the natural compound α-hederin in human colon cancer cells. We treated SW620 cells with interleukin-6 (IL-6) in vitro to mimic the paracrine inflammatory microenvironment of tumor cells. α-Hederin concentration dependently reduced the viability of IL-6-stimulated SW620 cells. α-Hederin increased the number of IL-6-stimulated SW620 cells at the G2/M phase and reduced the mRNA and protein expression of cyclin B1 and CDK1. Moreover, α-hederin induced apoptosis and loss of mitochondrial membrane potential in IL-6-stimulated SW620 cells. α-Hederin downregulated Bcl-2 expression, upregulated Bax expression, and promoted cytochrome c release from mitochondria into cytoplasm. Additionally, α-hederin elevated the levels of cleaved-caspase-9, cleaved-caspase-3, and cleaved-PARP, but had little effects on the levels of cleaved-caspase-8. Moreover, α-hederin prevented the nuclear translocation of nuclear factor-κB (NF-κB) and reduced the phosphorylation of IκBα and IKKα, suggesting the blockade of NF-κB signaling. NF-κB inhibitor PDTC not only produced similar proapoptotic effects on IL-6-stimulated SW620 cells as α-hederin did, but also synergistically enhanced α-hederin’s proapoptotic effects. Furthermore, α-hederin inhibited the phosphorylation of ERK in IL-6-stimulated SW620 cells, which was involved in α-hederin blockade of NF-κB nuclear translocation. Altogether, α-hederin suppressed viability, induced G2/M cell cycle arrest, and stimulated mitochondrial and caspase-dependent apoptosis in colon cancer cells, which were associated with disruption of NF-κB and ERK pathways, suggesting α-hederin as a promising candidate for intervention of colon cancer.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
    refInfo:
    holdings:
      @attributes:
        islocal: N