Dr. Agoulnik comes to FIU from the Baylor College of Medicine where she was an assistant professor in the Department of Molecular and Cellular Biology. She earned her Ph.D. at the Institute of Cytology and Genetics in Russia and did a postdoctoral fellowship at Baylor College of Medicine.

A cancer researcher and cell biologist, she is widely published in top academic journals on the subjects of prostate cancer and steroid receptor signaling. Her current research examines hormone resistance in prostate cancer. Hormone refractory prostate cancer, which occurs when hormone therapy fails to stop the growth of prostate cancer, is incurable and the main cause of death among prostate cancer patients. The research in Agoulnik's laboratory is supported by the National Cancer Institute and focused on the role of androgen receptor and its co-regulators in prostate cancer progression.

Research Interests:

To date prostate cancer remains the most common noncutaneous malignancy in men in the United States. Androgens and the androgen receptor (AR), play a crucial role in the development, differentiation and secretory function of the prostate gland. Deregulation of androgen receptor signaling and loss of androgen dependent growth of prostate epithelial cells are associated with prostate cancer development and progression. As such, therapies targeting the AR and AR signaling remain the cornerstone of therapeutic intervention in the management of advanced prostate tumors. In spite of the initial regression of tumors in response to androgen ablation therapies, tumors inevitably relapse and develop incurable castration resistant disease. My lab is focused on understanding the molecular and cellular changes that mediate the transition to castration resistant disease and the role AR signaling plays in this transition. Previously we have shown that the AR corergulators SRC-1 and SRC-2 (TIF2) are necessary for the stimulatory effect of androgens on proliferation and negatively correlate with patient survival. In addition, we and other groups have demonstrated that corepressors, such as NCoR, DAX-1, and SMRT are involved in both agonist and antagonist dependent regulation of AR action. We have shown that the AR corepressor NCoR plays a key role in the response to the anti-androgen casodex in AR-expressing prostate cancer cell lines. Thus underpinning the significant role of AR coregulators in modulating AR function in the development and progression of prostate cancer.

Most recently we identified the tumor suppressor gene INPP4B as a direct AR target gene in prostate cancer cells. INPP4B antagonizes oncogenic PIK3/Akt signaling, which is frequently hyperactive in prostate cancer, in addition to numerous other human malignancies. Loss of INPP4B accelerates prostate cancer cell proliferation and correlates with reduced time to biochemical recurrence and poor patient prognosis.

To further our understanding of the critical changes associated with castration resistant prostate cancer and nuclear receptor associated human diseases, we are currently employing selective mouse models of human disease in association with known cell based models. We are particularly focused on the role of AR regulated tumor suppressor gene INPP4B in both the maintenance of the differentiated state in normal prostate as well as their involvement in tumorigenesis. Our understanding of such pathways may elucidate critical biomarkers of disease and future therapeutic targets for the treatment of advanced prostate cancers.

Selected recent publications:

1. Agoulnik IU, Hodgson MC, Bowden WA, Ittmann MM. INPP4B: the new kid on the PI3K block. Oncotarget. 2011 Apr;2(4):321-8. (2011)
   
   
2. Hodgson MC, Shao LJ, Frolov A, Li R, Peterson LE, Ayala G, Ittmann MM, Weigel NL, Agoulnik IU. Decreased expression and androgen regulation of the tumor suppressor gene INPP4B in prostate cancer. Cancer Res, 71(2):572-82. (2011)
   
   
3. Feng S, Agoulnik IU, Truong A, Li Z, Creighton CJ, Kaftanovskaya EM, Pereira R, Han HD, Lopez-Berestein G, Klonisch T, Ittmann MM, Sood AK, Agoulnik AI. Suppression of relaxin receptor RXFP1 decreases prostate cancer growth and metastasis. Endocr Relat Cancer, 17(4):1021-33. (2010)
   
   
4. Agoulnik IU, Weigel, NL. Coactivator Selective Regulation of Androgen Receptor Activity. Steroids, , 74(8):669-74, (2009).
   
   
5. Agoulnik IU, Nakka M, Weigel NL. Target Gene Specific Regulation of Androgen Receptor Activity by p42/p44 MAPK. Mol Endo, 22(11):2420-32. (Nov. 2008).
   
   
6. Agoulnik IU, Weigel NL. Androgen receptor coactivators and prostate cancer. Adv Exp Med Biol, 617:245-55  (2008).
   
   
7. Agoulnik IU, Weigel NL. Androgen Receptor Coactivators and Prostate Cancer. Hormonal Carcinogenesis, Volume V. 5th International Symposium on Hormonal Carcinogenesis (2006).
   
   
8. Agoulnik IU, Vaid A, Nakka M, Alvarado M, Bingman WE III, Erdem H, Frolov A, Smith CL, Ayala G, Ittmann MM, Weigel NL. Androgen Receptor Coactivator TIF2 Expression, Biochemical Recurrence and Androgen Independence of Prostate Cancer. Cancer Research. 66:21; 10594-602  (Nov. 2006)
   
   
9. Agoulnik IU, Weigel NL. Androgen Receptor Action in Androgen Dependent and Recurrent Prostate Cancer. J Cell Biochem. 99:2;362-72  (Apr. 2006).
   
   
10. Dai H, Li R, Wheeler T, de Vivar AD, Chen X, Frolov A, Agoulnik IU, Thompson T, Rowley D, Ayala G. Pim-2 Upregulation: Biological Implications Associated with Perinueral Invasion and Disease Progression in Prostate Cancer. Prostate. 1:65;276-86 (Nov. 2005)
    
    
11. Agoulnik IU, Vaid A, Bingman WE III, Erdeme H, Frolov A, Smith CL, Ayala G, Ittmann MM, Weigel NL. A Role for SRC-1 in Promoting Prostate Cancer Cell Growth and Tumor Progression. Cancer Research. 1:65;7959-67  (Sep. 2005)