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Identification of Novel CK2 Kinase Substrates Using a Versatile Biochemical Approach
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Atypical protein kinase C phosphorylates IKKalphabeta in transformed non-malignant and malignant prostate cell

Hla Y Win1, Mildred Acevedo-Duncan

  • 1Department of Chemistry, University of South Florida, James A. Haley Veteran Hospital, 13000 Bruce B. Downs Blvd. VAR 151, Tampa, FL 33612, USA.

Cancer Letters
|June 24, 2008
PubMed

Insights

Atypical protein kinase C-iota (aPKC-iota) activation by tumor necrosis factor alpha (TNFalpha) influences the NF-kappaB pathway in prostate cells. This suggests aPKCs may regulate NF-kappaB signaling in prostate cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Atypical protein kinase C-iota (aPKC-iota) plays a role in cell survival and proliferation, making it a target in various cancers.
  • The NF-kappaB pathway is crucial in inflammation and cancer, and its regulation is of significant interest.

Purpose of the Study:

  • To investigate the role of aPKC-iota in the NF-kappaB pathway activation in prostate cancer cells treated with tumor necrosis factor alpha (TNFalpha).

Main Methods:

  • Prostate cancer cell lines (DU-145, RWPE-1, LNCaP) were treated with TNFalpha.
  • Western blotting and immunofluorescence were used to analyze protein phosphorylation, degradation, and nuclear translocation.

Main Results:

  • DU-145 cells showed TNFalpha-induced PKC-iota phosphorylation of IKKalphabeta, while RWPE-1 cells showed PKC-zeta involvement.
  • IkappaBalpha degradation and NF-kappaB/p65 nuclear translocation occurred in all cell lines.
  • LNCaP cells exhibited weak IKKalpha activation, with no observed upstream aPKC phosphorylation of IKKalphabeta.

Conclusions:

  • aPKCs may be involved in the activation of the NF-kappaB pathway in prostate cancer cells.
  • Differential roles of aPKC-iota and aPKC-zeta in TNFalpha-induced NF-kappaB signaling were observed across different prostate cell lines.

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