Targeting the Myristoylation of FRS2α Inhibits FGF/FGFRs‐mediated Oncogenic Signaling and Tumor Progression
Abstract
Fibroblast growth factor (FGF)/fibroblast growth factor receptor (FGFR) signaling facilitates tumor initiation and progression. Although there are currently approved inhibitors and agents in clinical trials targeting FGFR kinase activity that show therapeutic benefit, over‐expression and/or mutations of FGFRs eventually confer drug‐resistance and bypass the mechanisms of kinase inhibitors in a variety of cancer types. We hypothesize that a compound blocks the myristoylation of FRS2α, thus suppressing its interaction with FGFRs/FGFRsDRM and downstream proteins. As a result, it inhibits oncogenic signaling and tumor progression mediated by FGF/FGFRs or FGFRsDRM. The goal of this study is to investigate if the novel lead compound inhibits FGF/FGFRs oncogenic signaling and overcomes FGFRsDRM mediated drug resistance.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Apr 01, 2018
- Source ID
- 10.1096/fasebj.2018.32.1_supplement.804.2
Entities
People
- Houjian Cai
- Qianjin Li
Organizations
- National Institutes of Health
- United States Department of Defense
- University of Georgia