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Tyrosine protein kinase activity of human hyperplastic prostate and carcinoma cell lines PC3 and DU145

Y Durocher1, A Chapdelaine, S Chevalier

  • 1Maisonneuve-Rosemont Research Center, Montreal, Quebec, Canada.

Cancer Research
|September 1, 1989
PubMed

Insights

Tyrosine protein kinase (TPK) activity was detected in human benign prostatic hyperplasia (BPH) tissues and prostate cancer cell lines. This enzyme, crucial for cell signaling, was found in both soluble and particulate fractions, with higher specific activity in the latter.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Tyrosine protein kinases (TPKs) play critical roles in cellular signaling pathways.
  • Aberrant TPK activity is implicated in the development and progression of various cancers, including prostate cancer.
  • Understanding TPK expression and activity in benign prostatic hyperplasia (BPH) and prostate cancer is essential for therapeutic development.

Purpose of the Study:

  • To investigate the presence and characteristics of tyrosine protein kinase (TPK) in human benign prostatic hyperplasia (BPH) tissues and prostate cancer cell lines (PC3, DU145).
  • To compare TPK activity and localization in BPH tissues versus neoplastic cells.
  • To explore the enzymatic properties, substrate specificity, and molecular weight of TPKs in these biological samples.

Main Methods:

  • Utilized poly[Glu80Na,Tyr20] [poly(GT)] as a substrate for TPK detection.
  • Employed autoradiographic detection of alkali-resistant phosphoproteins after SDS-PAGE.
  • Fractionated tissue and cell extracts into soluble and particulate components for differential enzyme activity assessment.
  • Performed gel filtration chromatography (Sephacryl S-300) for preliminary molecular weight characterization of TPKs.

Main Results:

  • TPK activity was identified in human BPH tissues and PC3/DU145 prostate cancer cell lines.
  • The enzyme was predominantly found in soluble fractions of BPH tissues and Triton extracts of cell lines.
  • Specific TPK activity was higher in particulate fractions of BPH tissues compared to soluble fractions.
  • No significant TPK activity was detected in seminal plasma or sera from normal individuals or cancer patients.
  • TPK activity in human spermatozoa was significantly lower than in BPH tissue fractions.
  • TPK activity was dependent on Mn2+ or Mg2+ and abolished by heat denaturation.
  • Poly(GT) was a superior substrate compared to angiotensin II, casein, and histone H2B.
  • TPK activity was not stimulated by EGF, insulin, dihydrotestosterone, or estradiol.
  • Autoradiography revealed multiple alkali-resistant phosphoprotein bands (17,000–200,000 Da) in BPH tissues and neoplastic cells.
  • Soluble TPK from BPH tissues exhibited a molecular weight of approximately 50,000 Da, while particulate-associated TPK eluted with proteins of Mr 210,000.
  • Endogenous phosphorylation by peak fractions indicated major phosphoproteins in the 40,000–60,000 Da range.

Conclusions:

  • TPKs are expressed in both benign hyperplastic prostate tissues and prostate carcinoma cell lines.
  • BPH tissues exhibit at least two forms of TPK, with a predominant soluble enzyme of lower molecular weight (40,000–60,000 Da).
  • The findings suggest distinct TPK profiles in benign versus malignant prostate conditions, warranting further investigation.
  • TPK activity is not a reliable biomarker in seminal plasma or serum for prostate conditions.
  • The characterized TPKs may represent potential targets for therapeutic intervention in prostate diseases.

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