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Originally published In Press as doi:10.1074/jbc.M204405200 on July 30, 2002

J. Biol. Chem., Vol. 277, Issue 43, 41220-41229, October 25, 2002
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The Expression of novH in Adrenocortical Cells Is Down-regulated by TGFbeta 1 through c-Jun in a Smad-independent Manner*

Jérôme LafontDagger , Maryvonne LaurentDagger , Hélène ThiboutDagger , François Lallemand§, Yves Le BoucDagger , Azeddine Atfi§, and Cécile MartinerieDagger

From Dagger  INSERM U515 and § INSERM U482, Hôpital Saint-Antoine, 75571 Paris Cedex 12, France

The human NOV secreted glycoprotein (NOVH) is abundant in the fetal and adult adrenal cortex. The amount of NOVH increases in benign adrenocortical tumors and decreases in malignant adrenocortical tumors, suggesting that NOVH plays a role in tumorigenesis in the adrenal cortex. Transforming growth factor beta 1 (TGFbeta 1), fibroblast growth factor 2 (FGF2), and insulin growth factors (IGFs) play crucial roles in the physiology of the adrenal cortex. We investigated the effects of these factors on the expression of novH in the NCI H295R adrenocortical cell line. The amounts of NOVH protein and novH transcripts were down-regulated by TGFbeta 1 and up-regulated by FGF2, whereas IGFs had no effect. Furthermore, the TGFbeta 1-dependent inhibition of novH promoter activity was completely abrogated following site-directed mutation of two activating protein (AP-1) sequences (positions -473 and -447), whereas the stimulatory effect of FGF2 was not affected. Co-transfection with dominant negative forms of c-Jun and MEKK1 also abrogated novH-targeted regulation by TGFbeta 1, whereas the overproduction of Smad proteins or dominant negative forms of Smad had no effect. Taken together, these results suggest that c-Jun and MEKK1 signaling but not Smad signaling are involved in the TGFbeta 1-dependent decrease in NOVH in NCI H295R cells. In conclusion, our data provide evidence that novH is a new target of TGFbeta 1; unlike other members of the CCN (cyr61, ctgf, nov) family, however, its expression is repressed rather than induced.

* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EBI Data Bank with accession number(s) AJ431713.

To whom correspondence should be addressed: INSERM U515, Hôpital Saint-Antoine, 184 rue du Faubourg Saint-Antoine, 75571 Paris Cedex 12, France. Tel.: 33-1-4928-4664 or 4631; Fax: 33-1-4343-1065; Email: martiner@st-antoine.inserm.fr.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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