A novel model for metastasis suppression involving regulation of nuclear precursor mRNA stability

B. R. Henderson*, D. McDonald, S. Jones, R. F. Kefford

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Our previous data correlated urokinase plasminogen activator (uPA) gene activation with metastasis in different rat mammary carcinomas. However, inconsistent with this was the suppression of the uPA gene in the metastatic rat mammary carcinoma cell line, BC1. We have now re-examined this cell line, selecting in vivo specifically for those BC1 cells capable of lung metastasis. We demonstrate that within the polyclonal BC1 cell line, it is possible to enrich for a metastatic sub-population which synthesizes 4 to 5-fold higher levels of uPA mRNA and enzyme activity. Therefore, the ability of a BC1 cell to metastasize appears to correlate with its escape from suppression of the uPA gene in this tumour. The results are consistent with the mechanism of uPA gene activation in metastatic DMBA-8 rat mammary tumour cells, and suggest a novel model of tumour progression based on regulation of pre-mRNA stability.

Original languageEnglish
Pages (from-to)483-486
Number of pages4
JournalInternational Journal of Oncology
Volume6
Issue number2
Publication statusPublished - 1995
Externally publishedYes

Keywords

  • Metastasis
  • Nucleus
  • Precursor mRNA stability
  • Urokinase plasminogen activator

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