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Oncostatin M-mediated Transcriptional Suppression of the c-myc Gene in Breast Cancer Cells¹

Veterans Affairs Medical Center, Boise, Idaho 83702 [M. J. S., R. E. V., J. L.]; Mountain States Medical Research Institute, Boise, Idaho 83702 [M. J. S., R. E. V., J. L.]; and Departments of Medicine and Pharmacology, University of Washington, Seattle, Washington 98195 [R. E. V.]

Oncostatin M (OM) inhibits proliferation of H3922, a human breast cancer cell line derived from a ductal infiltrating carcinoma. We have found that treatment of H3922 cells with OM for 72 h lowers the steadystate level of c-myc mRNA to 16% of that seen in control cells. Our present study showed that down-regulation of c-myc mRNA levels was both dose and time dependent. Results from nuclear run-off analysis and mRNA stability studies established that a major component of the observed OM-induced down-regulation of c-myc mRNA occurs at the transcriptional level. OM treatment of H3922 cells reduced the abundance of actively transcribed c-myc mRNAs to approximately 25% of that observed in control cells. These data were supported by our finding that OM did not significantly affect the half-life of c-myc mRNA in actinomycin-treated H3922 cells. Taken together, these data demonstrate that the suppressive effect of OM on c-myc gene expression in H3922 cells occurs at the transcriptional level.

¹ Supported by the Mountain States Medical Research Institute, Boise, ID and by Grant AIBS 182 from the United States Army Medical Research and Development Command.

² To whom requests for reprints should be addressed, at Research Service (151), Veterans Affairs Medical Center, 500 West Fort Street, Boise, ID 83702-4598. Phone: (208) 422-1152 Fax: (208) 422-1155; E-mail: jingliu@micron.net.

Received 8/ 8/96. Accepted 4/ 1/97.

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