Suppression of Prostate Cancer

NIH RePORTER · NIH · R21 · $236,050 · view on reporter.nih.gov ↗

Abstract

Project Summary As many as 20% of aggressive prostate cancers have mutations resulting in upregulation of Wnt/β-catenin signaling. Importantly, recent analysis identified the Wnt/β-catenin pathway as the foremost differentially modulated pathway among treatment-resistant individuals. We used structure-based design of peptidomimetic oligomers to discover new molecules capable of inhibiting Wnt/β-catenin signaling and prostate cancer cell growth. We identified macrocycle 13 as a potent inhibitor of Wnt/β-catenin signaling. In this proposal we outline a strategy to use macrocycle 13 in models of castration resistant prostate cancer (CPRC) and to explore the biology of Wnt/β-catenin in prostate cancer. The hypothesis underlying of this project is that oligomer macrocycles can be rationally designed to inhibit the β-catenin/TCF interaction, thereby inhibiting prostate cancer tumor growth. Our specific aims are to 1) test macrocycle 13 inhibition of -catenin/TCF in in vivo models of aggressive prostate cancer and 2) determine macrocycle 13/β-catenin binding characteristics. Altogether, we expect that completion of our research goals will provide new molecular insight into Wnt/β- catenin signaling in prostate cancer.

Key facts

NIH application ID
10512253
Project number
1R21CA262963-01A1
Recipient
NEW YORK UNIVERSITY SCHOOL OF MEDICINE
Principal Investigator
Susan K. Logan
Activity code
R21
Funding institute
NIH
Fiscal year
2022
Award amount
$236,050
Award type
1
Project period
2022-09-01 → 2024-08-31