ArticleCell communication and signaling : CCS2019
Abi1 loss drives prostate tumorigenesis through activation of EMT and non-canonical WNT signaling.
Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
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- A system-wide investigation into the phosphoregulatory network of TNIK and its cellular implications.Frontiers in bioinformatics · 2026Article
- WNT signaling in cancer: molecular mechanisms and potential therapies.Molecular biomedicine · 2025Review
- Study of the role of transmembrane emp24 domain-containing protein 2 in oral squamous cell carcinoma.Journal of applied oral science : revista FOB · 2025Article
- Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024Review
- Frizzled receptors (FZDs) in Wnt signaling: potential therapeutic targets for human cancers.Acta pharmacologica Sinica · 2024Review
- Prostate Cancer Risk Stratification by Digital Histopathology and Deep Learning.JCO clinical cancer informatics · 2024Article
- Transcending frontiers in prostate cancer: the role of oncometabolites on epigenetic regulation, CSCs, and tumor microenvironment to identify new therapeutic strategies.Cell communication and signaling : CCS · 2024Review
- Impact of cell plasticity on prostate tumor heterogeneity and therapeutic response.American journal of clinical and experimental urology · 2024Review
- Pan-cancer transcriptomic data of ABI1 transcript variants and molecular constitutive elements identifies novel cancer metastatic and prognostic biomarkers.Cancer biomarkers : section A of Disease markers · 2024Article
- Recent Advances and Mechanism of Nanomaterials Promoting Tumor Metastasis.Environment & health (Washington, D.C.) · 2023Review
- Proximity proteomics reveals role of Abelson interactor 1 in the regulation of TAK1/RIPK1 signaling.Molecular oncology · 2023Article
- WAVE facilitates polarized E-cadherin transport.Molecular biology of the cell · 2023Article
- Epithelial-to-Mesenchymal Transition-Related Markers in Prostate Cancer: From Bench to Bedside.Cancers · 2023Review
- Abl kinases can function as suppressors of tumor progression and metastasis.Frontiers in oncology · 2023Article
- In Vivo Models for Prostate Cancer Research.Cancers · 2022Review
- ABI1-based expression signature predicts breast cancer metastasis and survival.Molecular oncology · 2022Article
- GPX2 predicts recurrence-free survival and triggers the Wnt/β-catenin/EMT pathway in prostate cancer.PeerJ · 2022Article
- Article
- The pattern of alternative splicing in lung adenocarcinoma shows novel events correlated with tumorigenesis and immune microenvironment.BMC pulmonary medicine · 2021Article
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Authors and funding
19 authors at 7 institutions in 4 countries.
Funding
Abstract
backgroundProstate cancer development involves various mechanisms, which are poorly understood but pointing to epithelial mesenchymal transition (EMT) as the key mechanism in progression to metastatic disease. ABI1, a member of WAVE complex and actin cytoskeleton regulator and adaptor protein, acts as tumor suppressor in prostate cancer but the role of ABI1 in EMT is not clear.
methodsTo investigate the molecular mechanism by which loss of ABI1 contributes to tumor progression, we disrupted the ABI1 gene in the benign prostate epithelial RWPE-1 cell line and determined its phenotype. Levels of ABI1 expression in prostate organoid tumor cell lines was evaluated by Western blotting and RNA sequencing. ABI1 expression and its association with prostate tumor grade was evaluated in a TMA cohort of 505 patients and metastatic cell lines.
resultsLow ABI1 expression is associated with biochemical recurrence, metastasis and death (p = 0.038). Moreover, ABI1 expression was significantly decreased in Gleason pattern 5 vs. pattern 4 (p = 0.0025) and 3 (p = 0.0012), indicating an association between low ABI1 expression and highly invasive prostate tumors. Disruption of ABI1 gene in RWPE-1 cell line resulted in gain of an invasive phenotype, which was characterized by a loss of cell-cell adhesion markers and increased migratory ability of RWPE-1 spheroids. Through RNA sequencing and protein expression analysis, we discovered that ABI1 loss leads to activation of non-canonical WNT signaling and EMT pathways, which are rescued by re-expression of ABI1. Furthermore, an increase in STAT3 phosphorylation upon ABI1 inactivation and the evidence of a high-affinity interaction between the FYN SH2 domain and ABI1 pY421 support a model in which ABI1 acts as a gatekeeper of non-canonical WNT-EMT pathway activation downstream of the FZD2 receptor.
conclusionsABI1 controls prostate tumor progression and epithelial plasticity through regulation of EMT-WNT pathway. Here we discovered that ABI1 inhibits EMT through suppressing FYN-STAT3 activation downstream from non-canonical WNT signaling thus providing a novel mechanism of prostate tumor suppression.
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