3,3',4', 5'-Tetramethoxychalcone inhibits human oral cancer cell proliferation and migration via p53-mediated mitochondrial-dependent apoptosis

Anticancer Res. 2014 Apr;34(4):1811-9.

Abstract

Background/aim: The current study aimed to identify an attractive target against human oral squamous cell carcinoma (OSCC).

Materials and methods: The effect of 3,3',4',5'-tetramethoxychalcone (TMC) on OSCC cell proliferation, cell-cycle phase distribution, expression of markers of cell apoptosis, and cell migration were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, western blot, and transwell migration assay, respectively.

Results: Experimental results revealed that TMC inhibited the OSCC cell proliferation (fifty percent inhibitory concentrations range=1.0-4.5 μM) by inducing G2/M phase arrest of the cell cycle. TMC caused DNA double-strand breaks, and enhanced expression of caspase-3 and -9, poly (ADP-ribose) polymerase, cytochrome c, calpain-1 and -2, phosphorylation of histone H2AX, phosphorylation of checkpoint kinases 2, p53, BCL2-antagonist/killer and BCL2-associated × protein, while reducing the mitochondrial membrane potential, and expression of B-cell lymphoma-2. In addition, TMC reduced the migration potential of OSCC cells by attenuating the C-C chemokine ligand 5/C-C chemokine receptor type 5 axis.

Conclusion: These data indicate that TMC may be considered an interesting target for further development of chemotherapeutic agents against oral cancer.

Keywords: 3,3’,4’,5’-tetramethoxychalcone; CCL5/CCR5 axis; DNA double-strand breaks; Oral cancer; apoptosis; cell migration; cell proliferation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / chemistry
  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Cell Movement / drug effects*
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Chalcone / analogs & derivatives
  • Chalcone / chemistry
  • Chalcone / pharmacology*
  • Chemokine CCL5 / metabolism
  • DNA Breaks, Double-Stranded / drug effects
  • Dose-Response Relationship, Drug
  • Humans
  • Membrane Potential, Mitochondrial / drug effects
  • Mitochondria / metabolism*
  • Mouth Neoplasms / metabolism*
  • Mouth Neoplasms / pathology
  • Receptors, CCR5 / metabolism
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Antineoplastic Agents
  • Chemokine CCL5
  • Receptors, CCR5
  • Tumor Suppressor Protein p53
  • Chalcone