Expression of protein kinase C isoenzymes in benign hyperplasia and carcinoma of prostate

Rumelia Koren*, David Ben Meir, Leah Langzam, Yoram Dekel, Miriam Konichezky, Jacob Baniel, Pinhas M. Livne, Rivka Gal, Sanford R. Sampson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

67 Scopus citations


Protein kinase C family consists of 11 isoforms, classified into 3 categories according to their structure and mechanisms of activation. These isoenzymes are involved in processes, which maintain intracellular homeostasis. Alterations in activity, amount or distribution of protein kinase C (PKC) isoenzymes may cause cellular proliferation or induce apoptosis. We have studied and compared the expression levels of several PKC isoforms in benign prostatic hyperplasia (BPH) and prostate cancer (PCa). These are PKCs α (alpha), β (beta), δ (delta), ε (epsilon), ζ (zeta), η (eta), which have been detected as major isoforms in prostate tissue. Paraffin sections of 25 benign prostatic hyperplasia (BPH) and 25 of prostatic carcinoma (PCa) were examined for expression of PKC α, β, δ, ε, ζ, and η. Expression of PKC β was examined in additional 3 BPH and 3 PCa using Western blot analysis. We found a significant high level of expression of PKC isoforms α, β, ε and η in PCa compared to BPH (p<0.01). Using backward logistic regression, we found changes in PKC ε expression to be most significant between malignant compared to benign tumor tissue specimens. Immunostaining for PKCs α, β and η in addition to PKC E may aid in distinguishing between benign and malignant prostatic disease.

Original languageEnglish
Pages (from-to)321-326
Number of pages6
JournalOncology Reports
Issue number2
StatePublished - Feb 2004


  • Benign prostatic hyperplasia
  • Prostate cancer
  • Protein kinase C


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