| Literature DB >> 34616876 |
Samuel J Rodgers1, Sabryn A Hamila1, Christina A Mitchell1, Lisa M Ooms1.
Abstract
AKT is the central phosphoinositide 3-kinase (PI3K) signaling effector, however, PIK3CA (p110α subunit of PI3Kα)-mutant estrogen receptor-positive (ER+) breast cancers exhibit minimal AKT activation and the downstream signaling is poorly characterized. We discovered that a subset of PIK3CA-mutant ER+ breast cancers exhibit increased inositol polyphosphate 4-phosphatase type II (INPP4B) expression, which promotes late endosome formation and glycogen synthase kinase 3 beta (GSK3β) trafficking, leading to enhanced Wingless-related integration site (WNT)/catenin beta 1 (β-catenin) activation.Entities:
Keywords: INPP4B; PIK3CA; WNT/β-catenin; cell proliferation; late endosome
Year: 2021 PMID: 34616876 PMCID: PMC8489923 DOI: 10.1080/23723556.2021.1954470
Source DB: PubMed Journal: Mol Cell Oncol ISSN: 2372-3556