Riccardin D-26, a synthesized macrocyclic bisbibenzyl compound, inhibits human oral squamous carcinoma cells KB and KB/VCR: In vitro and in vivo studies

Biochim Biophys Acta. 2013 Jan;1830(1):2194-203. doi: 10.1016/j.bbagen.2012.10.011. Epub 2012 Oct 17.

Abstract

Background: Riccardin D-26, a synthesized macrocyclic bisbibenzyl compound, might possess anti-cancer properties. We aimed to evaluate the efficacy of Riccardin D-26 as a candidate compound for treatment of cancers with sensitive or drug resistant cells.

Methods: Experiments were performed on human oral squamous carcinoma KB cells and vincristin-selected MDR KB/VCR cells. The inhibition of cell growth was evaluated by colorimetric and clonogenic assays. The apoptotic cells were determined by the Annexin V-FITC/PI staining assay. JC-1 fluorescence probe was used to examine the mitochondria membrane potential (MMP). Further experiments were performed in nude mice bearing KB or KB/VCR xenografts. Riccardin D-26 was administered by injection for 2weeks. The specimens of KB and KB/VCR xenografts were removed for TUNEL staining and Western blotting analysis.

Results: Riccardin D-26 significantly inhibited cancer growth in both KB and KB/VCR cells. Riccardin D-26's activity in cancer cells was greater than that in human normal liver cells. In mice, Riccardin D-26 effectively prevented the growth of KB and KB/VCR xenografts without significant toxicity. Further studies suggested that Riccardin D-26 inhibited cancer growth by inducing apoptosis in the activation of mitochondria-mediated intrinsic apoptosis pathway. Riccardin D-26 also possessed this activity in regulation of mitogen-related protein kinases such as MAPK and PI3K/Akt, which is associated with its inhibitory effect on KB/VCR cells.

Conclusions: Riccardin D-26 possessed an anti-proliferation activity against both sensitive KB and MDR KB/VCR cancer cells.

General significance: Riccardin D-26 could be a promising agent for treatment of cancers with sensitive or drug resistant cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Annexin A5 / metabolism
  • Antineoplastic Agents* / chemical synthesis
  • Antineoplastic Agents* / chemistry
  • Antineoplastic Agents* / pharmacology
  • Carcinoma, Squamous Cell / drug therapy*
  • Carcinoma, Squamous Cell / metabolism
  • Carcinoma, Squamous Cell / pathology
  • Cell Line, Tumor
  • Drug Resistance, Neoplasm / drug effects*
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Humans
  • Macrocyclic Compounds* / chemical synthesis
  • Macrocyclic Compounds* / chemistry
  • Macrocyclic Compounds* / pharmacology
  • Membrane Potential, Mitochondrial / drug effects
  • Mice
  • Mice, Nude
  • Mitochondria / metabolism
  • Mitochondria / pathology
  • Mitochondrial Membranes / metabolism
  • Mitochondrial Membranes / pathology
  • Mouth Neoplasms / drug therapy*
  • Mouth Neoplasms / metabolism
  • Mouth Neoplasms / pathology
  • Phenyl Ethers* / chemical synthesis
  • Phenyl Ethers* / chemistry
  • Phenyl Ethers* / pharmacology
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Stilbenes* / chemical synthesis
  • Stilbenes* / chemistry
  • Stilbenes* / pharmacology
  • Xenograft Model Antitumor Assays

Substances

  • Annexin A5
  • Antineoplastic Agents
  • Macrocyclic Compounds
  • Phenyl Ethers
  • Stilbenes
  • riccardin D
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases