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Stefin B, the major low molecular weight inhibitor in ovarian carcinoma

L Kastelic1, B Turk, N Kopitar-Jerala

  • 1Department of Biochemistry, Jozef Stefan Institute, Ljubljana, Slovenia.

Cancer Letters
|July 15, 1994
PubMed

Insights

Ovarian carcinomas exhibit elevated Stefin B levels, a cysteine proteinase inhibitor (CPI). Isolated ovarian Stefin B strongly inhibits cathepsin L, suggesting tumor CPIs function similarly to normal tissues.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Endogenous cysteine proteinase inhibitors (CPIs) regulate lysosomal cysteine endopeptidases (CPs).
  • Imbalances between CPs and CPIs are implicated in carcinomas.
  • Ovarian carcinomas show increased Stefin B and decreased Stefin A compared to normal tissue.

Purpose of the Study:

  • To isolate and characterize Stefin B from ovarian carcinoma.
  • To investigate the inhibitory properties of ovarian Stefin B against specific cathepsins.

Main Methods:

  • Isolation of Stefin B using affinity chromatography (Cm-papain Sepharose, anti-Stefin B-Sepharose 4B), gel filtration, and ion-exchange chromatography.
  • Characterization by SDS-PAGE and determination of isoelectric points (pI).
  • Enzyme inhibition assays to determine inhibition constants (Ki) against papain, cathepsin L, and cathepsin B.

Main Results:

  • Two major isoforms of ovarian Stefin B (pI 5.9 and 6.5) were isolated, with an Mr of approximately 14,000 and a blocked N-terminus.
  • Ovarian Stefin B strongly inhibited papain (Ki = 0.11 nM) and cathepsin L (Ki = 0.035 nM).
  • Moderate inhibition was observed for cathepsin B (Ki = 130 nM).

Conclusions:

  • The properties and inhibitory profile of ovarian Stefin B are comparable to Stefin B from other human and bovine sources.
  • Tumor-derived Stefin B likely functions similarly to its normal counterpart in regulating cysteine endopeptidases within the tumor microenvironment.

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