Apigenin inhibits HeLa sphere‑forming cells through inactivation of casein kinase 2α

  • Authors:
    • Jie Liu
    • Xiao‑Cheng Cao
    • Qiao Xiao
    • Mei‑Fang Quan
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  • Published online on: October 21, 2014     https://doi.org/10.3892/mmr.2014.2720
  • Pages: 665-669
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Abstract

The protein kinase casein kinase 2 (CK2) has been implicated in stem cell maintenance and its aberrant activation has been demonstrated in several types of cancer, including cervical cancer. In the present study, it was demonstrated that the sphere‑forming cells (SFCs) of HeLa cell lines exhibited self‑renewal capacity, indicating that they possessed the properties of cervical cancer stem‑like cells. HeLa‑derived SFCs exhibited a higher level of CK2α protein, compared with the parental cells. Apigenin, a dietary flavonoid, led to a dose‑dependent inhibition of the self‑renewal capacity and the protein expression of CK2α in HeLa‑derived SFCs. Furthermore, forced overexpression of CK2α resulted in a decrease in the inhibition of CK2α expression and the self‑renewal capacity induced by apigenin in HeLa‑derived SFCs. These results suggested that apigenin inhibits the self‑renewal capacity of HeLa‑derived SFCs through downregulation of CK2α expression.
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January-2015
Volume 11 Issue 1

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Spandidos Publications style
Liu J, Cao XC, Xiao Q and Quan MF: Apigenin inhibits HeLa sphere‑forming cells through inactivation of casein kinase 2α. Mol Med Rep 11: 665-669, 2015
APA
Liu, J., Cao, X., Xiao, Q., & Quan, M. (2015). Apigenin inhibits HeLa sphere‑forming cells through inactivation of casein kinase 2α. Molecular Medicine Reports, 11, 665-669. https://doi.org/10.3892/mmr.2014.2720
MLA
Liu, J., Cao, X., Xiao, Q., Quan, M."Apigenin inhibits HeLa sphere‑forming cells through inactivation of casein kinase 2α". Molecular Medicine Reports 11.1 (2015): 665-669.
Chicago
Liu, J., Cao, X., Xiao, Q., Quan, M."Apigenin inhibits HeLa sphere‑forming cells through inactivation of casein kinase 2α". Molecular Medicine Reports 11, no. 1 (2015): 665-669. https://doi.org/10.3892/mmr.2014.2720