ArticleOncotarget2016
Upregulated WDR26 serves as a scaffold to coordinate PI3K/ AKT pathway-driven breast cancer cell growth, migration, and invasion.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
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- Loss of RanBP9 cooperates with p53 deficiency to promote sarcomagenesis.Frontiers in oncology · 2026Article
- NovelFrontiers in pediatrics · 2026Article
- The many faces of the GID/CTLH E3 ligase complex.Biochemical Society transactions · 2025Review
- WDR26-related Skraban-Deardorff syndrome: clinical, genetic and pathomechanistic insights.European journal of medical research · 2025Article
- Unveiling RACK1: a key regulator of the PI3K/AKT pathway in prostate cancer development.Oncogene · 2025Article
- Combined Transcriptomic and Mendelian Randomisation Explores the Diagnostic Value of Ubiquitination-Related Genes in Sepsis.Journal of inflammation research · 2025Article
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- Exploring novel protein biomarkers for early-stage diagnosis and prognosis of T-acute lymphoblastic leukemia (T-ALL).Hematology, transfusion and cell therapy · 2024Article
- Genome-wide screen of Mycobacterium tuberculosis-infected macrophages revealed GID/CTLH complex-mediated modulation of bacterial growth.Nature communications · 2024Article
- Pooled endogenous protein tagging and recruitment for systematic profiling of protein function.Cell genomics · 2024Article
- Non-human primate model of long-COVID identifies immune associates of hyperglycemia.Nature communications · 2024Article
- Genome-wide CRISPR screens identify PTPN21 and WDR26 as modulators of the mitochondrial stress-induced ISR.Life metabolism · 2024Article
- Skraban-Deardorff intellectual disability syndrome-associated mutations in WDR26 impair CTLH E3 complex assembly.FEBS letters · 2024Article
- Novel loss-of-function variants inFrontiers in pediatrics · 2024Article
- LncRNA MALAT1 signaling pathway and clinical applications in overcome on cancers metastasis.Clinical and experimental medicine · 2023Review
- Pooled endogenous protein tagging and recruitment for scalable discovery of effectors for induced proximity therapeutics.Research square · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
The phosphatidylinositol 3-kinase (PI3K)/AKT pathway transmits signals downstream of receptor tyrosine kinases and G protein-coupled receptors (GPCRs), and is one of the most dysregulated pathways in breast cancer. PI3Ks and AKTs consist of multiple isoforms that play distinct and even opposite roles in breast cancer cell growth and metastasis. However, it remains unknown how the activities of various PI3K and AKT isoforms are coordinated during breast cancer progression. Previously, we showed WDR26 is a novel WD40 protein that binds Gβγ and promotes Gβγ signaling. Here, we demonstrate that WDR26 is overexpressed in highly malignant breast tumor cell lines and human breast cancer samples, and that WDR26 overexpression correlates with shortened survival of breast cancer patients. In highly malignant cell lines (MDA-MB231, DU4475 and BT549), downregulation of WDR26 expression selectively alleviated GPCR- but not EGF receptor-stimulated PI3K/AKT signaling and tumor cell growth, migration and invasion. In contrast, in a less malignant cell line (MCF7), WDR26 overexpression had the opposite effect. Additional studies indicate that downstream of GPCR stimulation, WDR26 serves as a scaffold that fosters assembly of a specific signaling complex consisting of Gβγ, PI3Kβ and AKT2. In an orthotopic xenograft mouse model of breast cancer, disrupting formation of this complex, by overexpressing WDR26 mutants in MDA-MB231 cells, abrogated PI3K/AKT activation and tumor cell growth and metastasis. Together, our results identify a novel mechanism regulating GPCR-dependent activation of the PI3K/AKT signaling axis in breast tumor cells, and pinpoint WDR26 as a potential therapeutic target for breast cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.