WDR26 in Advanced Breast Cancer: A Novel Regulator of the P13K/AKT Pathway
Abstract
The PI3K/AKT pathway is one of the most deregulated pathways in breast cancers (>70%), and a major contributor to tumor progression. PI3Ks and AKTs comprise of multiple isoforms that play a critical role in a wide variety of physiological progresses. Moreover, during cancer progression, different PI3K and AKT isoforms may have different and even opposite roles. Notably, PI3K and AKT2 have been identified as the major isoform that contribute to breast cancer growth and metastasis. Yet, it is not yet clear how to specifically target the PI3K/AKT2 without causing wide spread side effects. In this proposal, we aim to test the hypothesis that WDR26 functions as a novel regulator of the PI3K/AKT2 pathway, and a previously unidentified marker/therapeutic target in advanced breast cancer, in particular, triple negative breast cancer (TNBC). Our results thus far demonstrated that WDR26 selectively interacts with G, PI3K, and AKT2 and serves as a scaffold that fosters their interaction to promote PI3K/AKT activation; and in highly malignant and invasive breast tumors, upregulated WDR26 over activates the PI3K/AKT2 pathway, promoting breast tumor growth and metastasis. These findings thus pinpoint WDR26 as a potential therapeutic target for disrupting PI3K/AKT over activation and breast cancer progression.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2016
- Accession Number
- AD1025930
Entities
People
- Songhai Chen
Organizations
- University of Iowa