C. Jonat, H.J. Rahmsdorf, K.-K. Park, A.C.B. Cato, S. Gebel, H. Ponta, P. Herrlich, "Antitumor promotion and antiinflammation: down-modulation of AP-1 (Fos/Jun) activity by glucocorticoid hormone," Cell, 62:1189-1204, 1990.
Helmut Ponta (Kernforschungs-zentrum Karlsruhe, Germany):
"Our paper was the first in a series that show that members of the steroid receptor family and the transcription factor AP-1 (Fos/Jun) mutually interfere with each other without change in DNA occupancy. Thus, bona fide transcription factors possess functions in addition to binding to DNA and activating the RNA polymerase complex. This explains why bFGF, by activating Fos/Jun, blocks glucocorticoid-dependent adipocyte differentiation, or why retinoic acid can partially revert transformed cells. The anti-inflammatory action of glucocorticoids has been exploited in medical practice. Also, dexamethasone has been the prime antipromoting agent in mouse skin carcinogenesis. We have supplied a plausible mechanism: interference with the transcriptional program induced by phorbol ester tumor promoters or inflammatory mediators."