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© 1994 Oxford University Press

research-article

Permissivity for methotrexate-induced DHFR gene amplification correlates with the metastatic potential of rat adenocarcinoma cells

Christine Lücke-Huhle

Kernforschungszentrum Karlsruhe, Institut für Genetik Postfach 3640, D-76021 Karlsruhe, Germany

During selection for methotrexate (MTX) resistance the metastatic subclone BSp73ASML of a spontaneous rat adenocarcinoma and a metastatic transfectant containing the metastogene META-1 underwent amplification of the dihydrofolate reductase (DHFR) gene at accelerated rates in contrast to non-metastatic but closely related BSp73AS cells. A four log increase in MTX resistance was associated with a 16-fold amplification and increased expression of the DHFR gene. The capacity for gene amplification in metastatic BSp73ASML cells was correlated with a deletion in the p53 gene and enhanced expression of the oncogene c-myc due to a 10-fold amplification of the myc gene. Increased expression of Ki-ras and c-raf in the non-metastatic BSp73AS cells seen to confer tumorgenicity but not permissivity for gene amplification.


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