Heather Montie

About Heather Montie

Determining the role of the androgen receptor acetylation in prostate cancer
Prostate cancer is driven by the male hormones, androgens which mediate their activity through the androgen receptor (AR). Unfortunately most prostate cancerous tumors progressively become resistant to the preferred treatment modality, androgen deprivation therapy. This stage of treatment resistance is termed as Castration Resistant Prostate Cancer (CRPC). CRPC is usually the result of the over-activity of AR which becomes independent of the presence/absence of androgens and continues to drive aggressive growth of tumors. Due to its key role in promoting prostate cancer tumorigenesis in CRPC, it is essential to define efficient mechanisms for AR inhibition.

One of the mechanisms proposed to enhance the activity of AR in CRPC, even in the absence of androgens, is the addition of a small chemical group/moiety to the AR protein. This modification of AR is termed as acetylation and is proposed to convert the protein to a ‘super-AR’. However, there is currently no experimental data to show that AR acetylation directly enhances AR-dependent prostate cancer cell viability.

Dr. Heather Montie proposes to evaluate the role of AR acetylation in the enhanced AR functional activity central to CRPC. She will study the precise mechanisms by which this modification of AR enhances its cancer-promoting activity. Dr. Montie will also validate the potential of AR acetylation as a therapeutic target for castrate-resistant prostate cancer.