Biomedical Summer Undergraduate Research Experience Program (B-SURE)
The University of Texas Health Science Center at San Antonio (UTHSCSA)

CHATTERJEE, Bandana (Molecular Medicine):  Our laboratory has been studying how the androgen receptor, which is a gene-regulatory protein, functions to influence normal and aberrant cell growth and proliferation.   The androgen receptor normally resides in the cytoplasm as a functionally inactive protein.  The receptor is activated after it binds to its partner hormone, known generically as “androgen”.  The hormone-bound androgen receptor (AR) is then translocated to the nucleus where it regulates transcription of a whole array of genes that are known as androgen target genes.  The proteins encoded by the androgen target genes are involved in a broad spectrum of normal physiological processes such as spermatogenesis, male sexual development, skeletal growth, muscle mass development and brain function.  With chronic overexposure to androgen, target organs like the prostate and testis become susceptible to uncontrolled cell growth and proliferation, resulting in the development of tumor mass.  Our work focuses on the molecular mechanism that underlies altered target gene expression in response to the androgen receptor (AR)/androgen signaling.  We are also asking the question how this signaling pathway contributes to the development of prostate cancer.

        We have identified and characterized several androgen target genes whose transcription is either positively or negatively influenced by AR signaling.  We have also completed an in-depth analysis of the AR gene itself and made the observation that in several non-reproductive target tissues the expression of AR is down regulated during the process of aging. Transcription factors that coordinate this age-dependent down-regulation of AR includes Sp1, NFkB and a yet to be cloned nuclear factor called age-dependent factor (ADF).   One current focus in our laboratory is to clone the gene encoding the ADF protein and to characterize ADF activity.  In order to delineate the role of AR signaling in the development of prostate cancer, we have developed a novel transgenic mouse model in which a dual-gene approach allows highly amplified constitutive overproduction of AR in the prostate.   We have developed a second mouse model in which specific tumor suppressing proteins like p53 is functionally inactivated in the prostate in the background of AR overexpression.  We are currently investigating these mouse models for tumor development and for correlation between the altered profile in androgen target gene expression and pathological progression of prostate cancer.

Bandana Chatterjee's Research Web Page.