A role for the fyn oncogene in metastasis of methylcholanthrene‐induced fibrosarcoma a cells

Tetsuji Takayama, Yoshihiro Mogi, Katsuhisa Kogawa, Naohito Yoshizaki, Hirohito Muramatsu, Kazuhiko Koike, Kentaro Semba, Tadashi Yamamoto, Yoshiro Niitsu*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)

Abstract

Expression of various oncogenes (ras, myc, erbB2, src, fyn, yes and sis) in a high‐metastatic clone (MH‐02) derived from a murine methylcholanthrene‐induced fibrosarcoma A (Meth A) was compared with those of its parent clone (ML‐01) by Northern blot analysis. Two oncogenes, fyn, belonging to the tyrosine‐kinase family, and sis, belonging to the cellular‐growth‐factor family, were found to have higher signals (3.6‐fold and 1.8‐fold respectively) in MH‐02 than in ML‐01 cells. To explore the possibility that higher expression of these oncogenes is involved in enhanced metastasis of the MH‐02 clone, ML‐01 was transfected by a fyn vector and the metastatic potential of the transfectant was examined. Mice administered fyn‐transfected ML‐01 cells had significantly increased metastatic nodules in the lung, as compared with those whose ML‐01 cells were transfected with control vector without the fyn gene. The result indicates that the fyn gene is one of the factors governing the metastatic potential of Meth A cells.

Original languageGerman
Pages (from-to)875-879
Number of pages5
JournalInternational Journal of Cancer
Volume54
Issue number5
DOIs
Publication statusPublished - 1993 Jul 9
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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