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Inhibition of CK2 activity provokes different responses in hormone-sensitive and hormone-refractory prostate cancer

Andrea Hessenauer1, Mathias Montenarh, Claudia Götz

  • 1Medizinische Biochemie und Molekularbiologie, Universität des Saarlandes, D-66424 Homburg, Germany.

International Journal of Oncology
|May 10, 2003
PubMed

Insights

Protein kinase CK2 activity correlates with prostate cancer growth. While apigenin inhibited CK2 in both cell types, only hormone-sensitive cells underwent apoptosis, suggesting high CK2 activity is dispensable for hormone-refractory cancer growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Protein kinase CK2 (CK2) is implicated in cell growth and apoptosis.
  • Prostate carcinoma cell lines, LNCaP (hormone-sensitive) and PC-3 (hormone-refractory), exhibit distinct growth behaviors.

Purpose of the Study:

  • To investigate the role of CK2 in the differential growth and apoptosis of prostate cancer cell lines.
  • To determine the correlation between CK2 activity and prostate cancer cell properties.

Main Methods:

  • Comparative analysis of CK2 subunit levels and enzymatic activity in LNCaP and PC-3 cells.
  • Treatment with the flavonoid apigenin to assess its effect on CK2 activity and apoptosis induction.

Main Results:

  • CK2 subunit levels were similar, but enzymatic activity was significantly higher in hormone-refractory PC-3 cells compared to hormone-sensitive LNCaP cells.
  • Apigenin inhibited CK2 activity in both cell lines.
  • Only hormone-sensitive LNCaP cells exhibited apoptosis in response to apigenin treatment.

Conclusions:

  • A correlation exists between specific CK2 activity and the growth characteristics of prostate cancer cells.
  • High CK2 activity is not essential for the growth of hormone-refractory prostate cancer.
  • Elevated CK2 activity does not confer protection against apoptosis in hormone-refractory prostate cancer cells.

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