ArticlePloS one2014
Loss of Dab2 expression in breast cancer cells impairs their ability to deplete TGF-β and induce Tregs development via TGF-β.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Comparison Bioinformatic Analysis of Extracellular Vesicles-Related Genes and MicroRNAs in Breast Cancer.International journal of molecular sciences · 2025Article
- The scaffold protein disabled 2 (DAB2) and its role in tumor development and progression.Molecular biology reports · 2024Review
- Disable 2, A Versatile Tissue Matrix Multifunctional Scaffold Protein with Multifaceted Signaling: Unveiling Role in Breast Cancer for Therapeutic Revolution.Cell biochemistry and biophysics · 2024Review
- Identification and Validation of a Prognostic Signature Based on Methylation Profiles and Methylation-Driven GeneDisease markers · 2022Article
- Loss of Disabled-2 Expression in Pancreatic Cancer Progression.Scientific reports · 2019Article
- miR-106b targets DAB2 to promote hepatocellular carcinoma cell proliferation and metastasis.Oncology letters · 2018Article
- Switching Roles of TGF-β in Cancer Development: Implications for Therapeutic Target and Biomarker Studies.Journal of clinical medicine · 2016Review
- Integrin traffic - the update.Journal of cell science · 2015Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dab2 is a multifunctional adapter protein which is frequently under-expressed in a variety of cancers. It is implicated in many critical functions, including several signaling pathways, cell arrangement, differentiation of stem cells, and receptor endocytosis. Transforming growth factor-β (TGF-β) is a secreted multifunctional protein that controls several developmental processes and pathogenesis of many diseases. It has been documented that Dab2 played an important role in TGF-β receptors endocytosis. Here, we present evidence that re-expression of Dab2 in SK-BR-3 cell partially restored its ability to deplete TGF-β in surrounding medium by normalizing the trafficking of TGF-β receptors. We also demonstrate that the difference in TGF-β depletions produced by Dab2 expression was sufficient to impact on the conversion of naive CD4+ T cells to regulatory T cells (Tregs), and thus inhibited the proliferation of T cells. This work revealed a critical result that breast cancer cell was deficient in Dab2 expression and related receptor endocytosis-mediated TGF-β depletion, which may contribute to the accumulation of TGF-β in tumor microenvironment and the induction of immune tolerance.
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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.