REGULATORY EFFECTS OF POD-1/TCF21 ON STEROIDOGENIC FACTOR-1 (SF-1/NR5A1) IN PEDIATRIC AND ADULT ADRENOCORTICAL TUMOR CELLS

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 17-28-Adrenal Tumors & Pheochromocytoma
Basic/Clinical
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-28
Monica Malheiros França*1, Bruno Ferraz-de-Souza2, Mariza Gerdulo Santos3, Antonio Marcondes Lerario4, Maria Candida Barisson Villares Fragoso5, Ana Claudia Latronico6, Gary D Hammer7 and Claudimara Ferini Pacicco Lotfi8
1University of Sao Paulo, Sao Paulo, Brazil, 2Univ of Sao Paulo School of Medi, Sao Paulo, Brazil, 3HC FM Univ of Sao Paulo, Sao Paulo, Brazil, 4Hosp das Clinicas, Sao Paulo, Brazil, 5University of Sao Paulo, Sao Paulo-SP, Brazil, 6Hospital das Clinicas da Faculdade de Medicina da Universidade de São Paulo, Sao Paulo, Brazil, 7Univ of Michigan, Ann Arbor, MI, 8University of Sao Paulo, Sao Paulo SP, Brazil
REGULATORY EFFECTS OF POD-1/TCF21 ON STEROIDOGENIC FACTOR-1 (SF-1/NR5A1) IN PEDIATRIC AND ADULT ADRENOCORTICAL TUMOR CELLS

Monica Malheiros França1, Bruno Ferraz-de-Souza2, Mariza G. Santos3, Antonio M. Lerario3, Maria Candida B Villares Fragoso3, Ana Claudia Latronico3, Gary D. Hammer4, Claudimara F. Lotfi1

1Department of Anatomy, Biomedical Science Institute, 2Laboratory of Carbohydrates and Radioimmunoassays (LIM18); 3Laboratory of Molecular Genetics and Hormones (LIM42), School of Medicine; University of São Paulo, SP, Brazil, 4Department of Internal Medicine, Metabolism, Endocrinology and Diabetes, University of Michigan, USA.

Pod-1/Tcf21 has been showed to inhibit Sf-1 expression by antagonizing the activity of USF on the proximal E-box Sf-1 promoter site in Leydig cells. Also, an increase in Sf-1 expression was observed in Pod-1 deficient-Leydig cells. Recently, we have shown that POD-1 overexpression inhibits endogenous SF-1 expression through binding to the E-box sequence on SF-1 promoter in human adrenocortical tumor cells. Here, we detected cMYC and SF-1 protein in H295R and in an adult adrenocortical carcinoma cells (ACC-T36) transfected with pCMVMyc and pCMVMycPod-1. Furthermore, CYP11A1 gene expression was quantified in these H295R and ACC-T36 transfected cells. In addition, the expression of POD-1 and SF-1 was evaluated in pediatric adrenocortical tumor cells (ACT-T7 cells) transfected with siRNA targeting POD-1 by using qPCR. Our results show an increase of cMYC protein expression and a decrease of SF-1 protein in both H295R and ACC-T36 cells transfected with pCMVMycPod-1 in relation to control. Specifically we observed 0.77 ± 0.2 and 0.70 ± 0.1-fold decrease of CYP11A1 expression respectively in both cell lines when compared with the cells transfected with the empty plasmid. Preliminary results show 0.6-fold decrease of POD-1 expression and 9.2-fold increase of SF-1 expression in POD-1 knockdown of ACT-T7 cells transfected with siRNA-POD-1, in comparison with siRNAcontrol. In summary our results suggest a regulatory effect of POD-1 on SF-1 expression in both pediatric and adult adrenocortical tumor cells.

Nothing to Disclose: MMF, BF, MGS, AML, MCBVF, ACL, GDH, CFPL

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm

Sources of Research Support: MMF is recipient of scholaship from FAPESP and CFPL receveid funding from FAPESP, CAPES, CNPq and PrP-USP.
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