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Title: Selective expression of a splice variant of decay-accelerating factor in c-erbB-2-positive mammary carcinoma cells showing increased transendothelial invasiveness

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [1];  [2];  [3];  [1];  [1];  [2];  [4]
  1. Institute of Clinical Chemistry and Laboratory Medicine, University of Muenster (Germany)
  2. Institute of Pathology, University of Basel (Switzerland)
  3. Carpegen GmbH, Mendelstr. 11, 48149 Muenster (Germany)
  4. Institute of Pathology, University of Muenster (Germany)

By differential-display-PCR a subclone of the SK-BR-3 cell line with high in vitro transendothelial invasiveness was identified to express increased levels of a new alternative splice variant of decay-accelerating factor (DAF). DAF seems to play an important role in some malignant tumours since on the one hand the expression of complement inhibitors on the surface of tumour cells prevents the accumulation of complement factors and in consequence cell lysis. On the other hand, DAF has been identified as a ligand for the CD97 surface receptor which induces cell migration. Immunofluorescence procedures, Western blot analyses, and cDNA clone sequencing were employed to confirm the expression of DAF restricted to invasive tumour cells. Using a radioactive RNA-in situ hybridisation on freshly frozen tissue microarrays and RT-PCR on native tumour tissue, the expression of alternative spliced DAF mRNA was demonstrated in invasive breast cancer. Due to the fact that it could thereby not be detected in normal mammary tissues, it has to be confirmed in larger studies that the DAF splice variant might be a specific tumour marker for invasive breast cancer.

OSTI ID:
20630911
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 329, Issue 1; Other Information: DOI: 10.1016/j.bbrc.2005.01.138; PII: S0006-291X(05)00157-9; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English