Apoptotic effects of 7,8-dihydroxyflavone in human oral squamous cancer cells through suppression of Sp1

Oncol Rep. 2015 Feb;33(2):631-8. doi: 10.3892/or.2014.3632. Epub 2014 Nov 27.

Abstract

7,8-Dihydroxyflavone (7,8-DHF) is a member of the flavonoid family and has recently been identified as a brain-derived neurotrophic factor mimetic that selectively activates tropomyosin-receptor kinase B with high affinity. The antioxidant and anticancer effects of 7,8-DHF have been reported. However, the pharmacological mechanisms of 7,8-DHF in oral cancer are unclear. Thus, we investigated the mechanisms of the antiproliferative action of 7,8-DHF on HN22 and HSC4 oral squamous cell carcinoma cell lines. We demonstrated that 7,8-DHF decreased cell growth and induced apoptosis in the HN22 and HSC4 cells through regulation of specificity protein 1 (Sp1) using the MTS assay, DAPI staining, Annexin V, propidium iodide staining, reverse transcription-polymerase chain reaction, immunocytochemistry, pull-down assay and western blot analysis. The results showed that the Sp1 protein bound with 7,8-DHF in the HN22 and HSC4 cells. Taken together, the results suggest that 7,8-DHF could modulate Sp1 transactivation and induce apoptotic cell death by regulating the cell cycle and suppressing antiapoptotic proteins. Furthermore, 7,8-DHF may be valuable for cancer prevention and better clinical outcomes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis
  • Carcinoma, Squamous Cell / metabolism*
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Flavones / pharmacology*
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Mouth Neoplasms / metabolism*
  • Sp1 Transcription Factor / metabolism*

Substances

  • 6,7-dihydroxyflavone
  • Antineoplastic Agents
  • Flavones
  • Sp1 Transcription Factor
  • SP1 protein, human