Cancer Institute

  • Damian G. Romero

    romero_damian.jpgAssociate Professor, Department of Biochemistry
    Tumor Cell Biology Program
    PhD, Molecular Biology, 2000, University of Buenos Aires, Argentina
    Postdoc, 2000-08, University of Mississippi Medical Center, Jackson, MS

    Contact information
    2500 N State St., Room G206
    Jackson, MS 39216
    Phone: (601) 984-1523
    E-mail: dromero@umc.edu

    Research interests

    • Regulator of G-protein signaling (RGS) proteins and breast cancer
    • Renin-Angiotensin-Aldosterone system and breast cancer

    Research synopsis

    Breast cancer is the most common cancer and the second leading cause of cancer related deaths in females. G-protein coupled receptors (GPCRs) have widespread fundamental roles in cellular signaling. Heterotrimeric G-proteins are the molecular switches that turn on intracellular signaling cascades in response to the activation of GPCRs by extracellular stimuli. Therefore, G proteins have a crucial role in defining the specificity and temporal characteristics of the cellular response. G-proteins are switched on by GTP binding, and intrinsic GTPase activity hydrolyzes G-protein bound GTP to GDP to return to the basal state. However, G-proteins GTPase activity is too low to account for the rapid changes in G-protein activation/deactivation status observed in vivo. Regulator of G-protein signaling (RGS) proteins increase G-proteins GTPase activity thousands of times. The RGS protein family is ubiquitously expressed and RGS proteins are involved in any intracellular signaling process in which GPCRs are involved.

    Although a highly attractive target, the role of RGS proteins in cancer is poorly understood. Screening for RGS proteins differentially expressed in MCF-7 breast cancer cells, which were grown in three dimensional extracellular matrixes that closely resemble the in vivo tumor microenvironment, we found that RGS22, the newest member of the RGS protein family, was significantly upregulated. Our studies have shown that RGS22 downregulation significantly decreases breast cancer cell proliferation, while RGS22 overexpression has the opposite effect. The recent development of specific RGS protein inhibitors makes RGS22 an exciting novel target to abolish or mitigate the exacerbated cell proliferation observed in breast cancers.

    Recent accomplishments and honors

    • 2008 Caroline tum Suden/Frances A. Hellebrandt Professional Opportunity Award, American Physiological Society
    • 2006 Mead-Johnson Research Award, American Physiological Society, Endocrinology and Metabolism Section

    Selected publications

    • Romero DG et al. Angiotensin II- Regulated Transcription Regulatory Genes in Adrenal Steroidogenesis. Physiol Genomics 42A:259-66, 2010.
    • Romero DG et al. MicroRNA-21 increases aldosterone secretion and proliferation in H295R human adrenocortical cells. Endocrinology 149:2477-83, 2008.
    • Romero DG et al. RGS4 in adrenal gland: localization, regulation and role in aldosterone secretion. J Endocrinology 194:429-40, 2007.
    • Romero DG et al. RGS2 is regulated by angiotensin II and functions as a negative feedback of aldosterone production in H295R human adrenocortical cells. Endocrinology 147:3889-97, 2006.
    • Romero DG et al. Angiotensin II-mediated protein kinase D activation stimulates aldosterone and cortisol secretion in H295R human adrenocortical cells. Endocrinology 147:6046-55, 2006.