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A role for the fyn oncogene in metastasis of methylcholanthrene‐induced fibrosarcoma a cells
Author(s) -
Takayama Tetsuji,
Mogi Yoshihiro,
Kogawa Katsuhisa,
Yoshizaki Naohito,
Muramatsu Hirohito,
Koike Kazuhiko,
Semba Kentaro,
Yamamoto Tadashi,
Niitsu Yoshiro
Publication year - 1993
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910540525
Subject(s) - methylcholanthrene , fibrosarcoma , fyn , metastasis , cancer research , medicine , pathology , biology , cancer , carcinogen , genetics , receptor , proto oncogene tyrosine protein kinase src
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.