ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009
Activated Abl kinase inhibits oncogenic transforming growth factor-beta signaling and tumorigenesis in mammary tumors.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 62 citations in OpenAlex.
- TGF-β upregulates miR-181a expression to promote breast cancer metastasis.The Journal of clinical investigation · 2013Trial
- Recent advances in Pyrazolo[3,4-d]pyrimidine-based dual inhibitors in the treatment of cancers.Molecular diversity · 2026Review
- Bend and Snap: Computationally Exploring the Helix Bias for Classifying Abl Kinase Allosteric Modulators.Journal of chemical information and modeling · 2026Article
- Resistance to Allosteric Inhibitors.Journal of molecular biology · 2025Review
- ABL1 kinase as a tumor suppressor in AML1-ETO and NUP98-PMX1 leukemias.Blood cancer journal · 2023Article
- Abl kinases can function as suppressors of tumor progression and metastasis.Frontiers in oncology · 2023Article
- PRR16/Largen Induces Epithelial-Mesenchymal Transition through the Interaction with ABI2 Leading to the Activation of ABL1 Kinase.Biomolecules & therapeutics · 2022Article
- A Conformation Selective Mode of Inhibiting SRC Improves Drug Efficacy and Tolerability.Cancer research · 2021Article
- Molecular insights on ABL kinase activation using tree-based machine learning models and molecular docking.Molecular diversity · 2021Article
- Role of the ABL tyrosine kinases in the epithelial-mesenchymal transition and the metastatic cascade.Cell communication and signaling : CCS · 2021Review
- Biomechanical regulation of breast cancer metastasis and progression.Scientific reports · 2021Article
- Review
- EnABLing Tumor Growth and Progression: Recent progress in unraveling the functions of ABL kinases in solid tumor cells.Current pharmacology reports · 2018Article
- Mutant p53 dictates the oncogenic activity of c-Abl in triple-negative breast cancers.Cell death & disease · 2017Article
- Opposing roles of KIT and ABL1 in the therapeutic response of gastrointestinal stromal tumor (GIST) cells to imatinib mesylate.Oncotarget · 2017Article
- α3β1 Integrin Suppresses Prostate Cancer Metastasis via Regulation of the Hippo Pathway.Cancer research · 2016Article
- c-Abl inhibits breast cancer tumorigenesis through reactivation of p53-mediated p21 expression.Oncotarget · 2016Article
- Rapid Discovery and Structure-Activity Relationships of Pyrazolopyrimidines That Potently Suppress Breast Cancer Cell Growth via SRC Kinase Inhibition with Exceptional Selectivity over ABL Kinase.Journal of medicinal chemistry · 2016Article
- Discovery of Bivalent Kinase Inhibitors via Enzyme-Templated Fragment Elaboration.ACS medicinal chemistry letters · 2015Article
- c-Abl antagonizes the YAP oncogenic function.Cell death and differentiation · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Transforming growth factor-beta (TGF-beta) is a ubiquitous cytokine with dual roles in tumor suppression and promotion, and these dichotomous functions have frustrated the development of therapies targeting oncogenic signaling by TGF-beta. In comparison, Abl is well established as an initiator of hematopoietic cancers; however, a clear role for Abl in regulating solid tumor development remains elusive. Here, we investigated the role of Abl in TGF-beta-mediated epithelial-mesenchymal transition (EMT) in normal and metastatic mammary epithelial cells (MECs). In doing so, we identified Abl as an essential regulator of MEC morphology and showed that Abl inactivation was sufficient to induce phenotypic and transcriptional EMT in normal MECs. Increasing Abl activity in metastatic MECs resulted in their complete morphological reversion, restored their cytostatic response to TGF-beta, and blocked their secretion of matrix metalloproteinases induced by TGF-beta. Constitutively active Abl expression blocked TGF-beta-responsive mammary tumor growth in mice, while Imatinib therapy afforded no clinical benefit in mice bearing mammary tumors. Collectively, this investigation establishes Abl as a potent mediator of MEC identity, and as a suppressor of oncogenic TGF-beta signaling during mammary tumorigenesis. Notably, our findings strongly caution against the use of pharmacological Abl antagonists in the treatment of developing and progressing mammary tumors.
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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.