Opposite expression of securin and γ-H2AX regulates baicalein-induced cancer cell death

Ren Huei Jiang, Wen Chi Su, Huei Fang Liu, Hou Syun Huang, Jui-I Chao*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


Securin and γ-H2AX have been shown to regulate cell survival and genomic stability. However, it is still unknown how the expression and regulation of these proteins is altered following treatment with baicalein, a natural flavonoid extracted from the Scutellaria baicalensis root. In the present study, we investigate the possible roles of securin and γ-H2AX in baicalein-induced cancer cell death. Baicalein reduced cell viability in a variety of human cancer cell lines, including bladder, cervical, colon, and lung cancer cells. Interestingly, baicalein treatment (40-80 μM for 24 h) markedly inhibited securin expression, while the levels of γ-H2AX were elevated. Abnormal spindle formation and chromosomal segregation were induced by baicalein. Furthermore, wild type HCT116 cancer cells had a higher incidence of cytotoxicity and apoptosis than securin-null HCT116 cells following treatment with baicalein. In contrast, baicalein increased the levels of γ-H2AX to a similar extent in both cell types. Transfection with H2AX siRNA further increased baicalein-induced cell death. Additionally, blockade of the AKT pathway by treatment with wortmannin or AKT shRNA lowered the levels of γ-H2AX and enhanced cytotoxicity in baicalein-treated cells. Taken together, our findings suggest that the opposing effects of baicalein on securin and γ-H2AX levels may be involved in the regulation of cell viability and genomic stability by this compound.

Original languageEnglish
Pages (from-to)274-283
Number of pages10
JournalJournal of Cellular Biochemistry
Issue number2
StatePublished - 1 Oct 2010


  • Γ-H2AX
  • AKT
  • Apoptosis
  • Baicalein
  • Cell Viability
  • Securin


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