Suma Datta received a B.S. in Cellular and Molecular Biology and B. Chem.(1980) from the University of Michigan-Ann Arbor and a Ph.D.(1987) in Biology from the University of California-San Diego. She held a postdoctoral position as an LSRF Fellow at Yale University with Dr. Douglas R. Kankel. She joined the Department of Biochemistry and Biophysics, with a joint appointment in the Department of Biology, at Texas A&M University in 1993. She was promoted to Associate Professor in 1999. She is a member of the Faculty of Genetics, and the Faculty of Neuroscience.

2128 TAMU
College Station, TX 77843-2128

Office:
Bio/Bio
Room 333A
979-862-4641

Lab:
Bio/Bio
Rooms 330, 333
979-862-4642

Fax: 979-845-9724
Email: sumad@tamu.edu

Prostate cancer is the third leading cause of death in men. More than 70% of all prostate cancers are diagnosed in men over the age of 65, rendering age the biggest risk factor for prostate cancer. Recent advances in prostate cancer research have implicated the deregulation of developmental signaling pathways as a major influence in the metastatic behavior of cancer. Changes in the cellular microenvironment, including the extracellular matrix, are known to play a crucial role in the regulation of many of these signaling pathways and their various effects. Studies by our group and others have revealed that the Sonic Hedgehog (SHH) signaling pathway increases proliferation and metastasis of advanced prostate cancer cells. We have further demonstrated that the extracellular matrix proteoglycan Perlecan regulates the level of SHH signaling in advanced prostate cancer cells. Co-localization of Perlecan and SHH in human samples correlates with high Gleason Grade, aggressive tumors. Furthermore, Perlecan regulates signaling by other growth factors, such as FGF2 and VEGF, which are also critical for cancer growth and progression. This suggests that up-regulation of Perlecan in advanced tumors results in dramatic changes in growth factor response by metastatic cells. We are currently investigating the mechanisms regulating increased Perlecan production in invasive and metastatic prostate cancer cells.

Initial insights about the nature of the Perlecan-SHH interaction were discovered in the fruit fly Drosophila, which has been successfully established as an aging model. In order to study the effects of aging on the composition of the cellular microenvironment and thus on signaling and cancer progression, we have developed a fly model for prostate cancer based on anatomical, physiological and molecular criteria. We have demonstrated that expression of the Drosophila Perlecan, trol, is regulated in an age-dependent manner, as is the SHH homolog hh and its response gene ptc. Finally, our prostate model shows induced overgrowth upon expression of oncogenic Rasv12 and spontaneous overgrowth with old age.

Barrett, A., Kreuger, S., Perry, T. L. and Datta, S. (2008). Curable genetic instability of a gal4 transgene in Drosophila. In revision for Fly.

Barrett, A., Kreuger, S. and Datta, S. (2008). Bnl and Hedgehog operate in a positive feedback loop to regulate the initiation of neuroblast division in the Drosophila larval brain. In press for Developmental Biology.

Lindner, J., Hillman, P., Barrett, A., Jackson, M., Perry, T., Park, Y. and Datta, S. (2007). The Drosophila Perlecan gene trol regulates multiple signaling pathways in different developmental contexts. BMC Developmental Biology, 7: 121.

Datta, S. Pierce, M. and Datta, M. (2006). Perlecan Signaling: Helping Hedgehog stimulate Prostate Cancer Growth. International Journal of Biochemistry and Cell Biology 38: 1855-1861.

Datta, M. W., Hernandez, A. M., Schlicht, M., Kahler, A. J., DeGueme, A. M., J., Dhir, R., Shah, R., Farach-Carson, M. C., Barrett, A. and Datta, S. (2006). Perlecan, a candidate gene for the CABP locus, regulates cancer cell growth via the Sonic Hedgehog pathway. Molecular Cancer 5(1): 9.

Datta, S. and Datta, M. (2006). Sonic Hedgehog signaling in advanced prostate cancer. Cellular and Molecular Life Sciences, 63:435-448.

Liu Y, Ahn JE, Datta S, Salzman RA, Moon J, Huyghues-Despointes B, Pittendrigh B, Murdock LL, Koiwa H, Zhu-Salzman K. (2005). Arabidopsis Vegetative Storage Protein Is an Anti-Insect Acid Phosphatase. Plant Physiol. 139: 1545-1556.

Sanchez, P., Hernández, A. M., Stecca, B., Kahler, A. J., DeGueme, A. M., Barrett, A., Beyna, M., Datta, M. W., Datta, S. and Ruiz i Altaba, A. (2004). Inhibition of prostate cancer proliferation by interference with Hedgehog-GLI1 signaling. Proc. Natl. Acad. Sci., 101: 12561-12566.

Park, Y., Ng, C. and Datta, S. (2003). Induction of String rescues the neuroblast proliferation defect in trol mutant animals. Genesis, 36(4): 187-195.

Park, Y., Rangel, C., Reynolds, M., Caldwell. M. C., Johns, M., Nayak, M., Welsh, C. J. R., McDermott, S. and Datta, S. (2003). Drosophila Perlecan modulates FGF and Hedgehog signals to activate stem cell division. Developmental Biology, 253(2): 247-257.

Park, Y., M. Fujioka, M. Kobayashi, J.B. Jaynes, and S. Datta. 2001. even-skipped is required to produce a trans-acting aignal for larval neuroblast proliferation that can be mimicked by ecdysone. Development 128(10): 1899-1909.

Datta, S. 1999. Activation of neuroblast proliferation in explant culture of Drosophila larval brains. Brain Research 818(1): 77-83.

Park, Y., M. Fujioka, J.B. Jaynes, and S. Datta. 1998. The Drosophila homeobox gene eve is an enhancer of trol, an activator of neuroblast proliferation in the larval CNS. Developmental Genetics, 23:247-257.

Caldwell, M.C. and S. Datta. 1998. Expression of cyclin E or DP/E2F rescues the G1 arrest of trol mutant neuroblasts in the Drosophila larval CNS. Mech. Devel, 79(1-2):121-130.

Park, Y., M.C. Caldwell, and S. Datta. 1997. Mutation of the CNS neuroblast proliferation repressor ana leads to defects in olfactory behavior. J. Neurobiology 33(2): 19-211.