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Updated: Aug 7, 2026

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
Published on: July 17, 2019
HuR degradation reveals dependencies in BRAF-driven cancers
Ivan R Siordia1, Jonathan R Brody1, Dan A Dixon2
1Department of Surgery, Oregon Health & Science University, Portland, OR, USA; Department of Cell, Developmental and Cancer Biology, Oregon Health & Science University, Portland, OR, USA; Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA; Brenden-Colson Center for Pancreatic Care, Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Researchers discovered a molecular glue that degrades HuR, a challenging RNA-binding protein target. This breakthrough suppresses BRAF-mutant colorectal cancer, offering a new therapeutic strategy for specific cancers.
Area of Science:
- Oncology
- Molecular Biology
- Drug Discovery
Background:
- Targeting RNA-binding proteins (RBPs) is difficult due to a lack of druggable pockets.
- Hu-antigen R (HuR) is an RBP implicated in various malignancies.
- BRAF-mutant colorectal cancer presents a significant therapeutic challenge.
Purpose of the Study:
- To identify novel therapeutic strategies for BRAF-mutant colorectal cancer.
- To explore the degradation of HuR as a potential cancer treatment.
- To investigate the efficacy of a newly identified molecular glue targeting HuR.
Main Methods:
- Identification of a novel molecular glue compound.
- Assessment of the compound's ability to degrade HuR.
- Evaluation of the compound's effect on BRAF-mutant colorectal cancer cell lines and xenografts.
Main Results:
- A molecular glue was identified that effectively degrades HuR.
- The compound demonstrated significant suppression of BRAF-mutant colorectal cancer growth.
- This targeted degradation offers a new approach for HuR-driven cancers.
Conclusions:
- Molecular glues represent a viable strategy for targeting previously undruggable RBPs like HuR.
- Degradation of HuR is a promising therapeutic avenue for BRAF-mutant colorectal cancer.
- This approach may be applicable to other HuR-dependent malignancies.
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