ArticleMolecular and cellular biology2008
Signaling through ShcA is required for transforming growth factor beta- and Neu/ErbB-2-induced breast cancer cell motility and invasion.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 63 citations in OpenAlex.
- HER2 phosphorylation induced by TGF-β promotes mammary morphogenesis and breast cancer progression.The Journal of cell biology · 2024Article
- The SHCA adapter protein cooperates with lipoma-preferred partner in the regulation of adhesion dynamics and invadopodia formation.The Journal of biological chemistry · 2020Article
- Shedding New Light on Cancer Metabolism: A Metabolic Tightrope Between Life and Death.Frontiers in oncology · 2020Review
- Role of TGF‑β in the motility of ShcD‑overexpressing 293 cells.Molecular medicine reports · 2019Article
- GPNMB augments Wnt-1 mediated breast tumor initiation and growth by enhancing PI3K/AKT/mTOR pathway signaling and β-catenin activity.Oncogene · 2019Article
- Emerging roles for LPP in metastatic cancer progression.Journal of cell communication and signaling · 2018Review
- Integrin-uPAR signaling leads to FRA-1 phosphorylation and enhanced breast cancer invasion.Breast cancer research : BCR · 2018Article
- MPZL1 forms a signalling complex with GRB2 adaptor and PTPN11 phosphatase in HER2-positive breast cancer cells.Scientific reports · 2017Article
- Two distinct mTORC2-dependent pathways converge on Rac1 to drive breast cancer metastasis.Breast cancer research : BCR · 2017Article
- The Cdc42/Rac1 regulator CdGAP is a novel E-cadherin transcriptional co-repressor with Zeb2 in breast cancer.Oncogene · 2017Article
- Insights into the Shc Family of Adaptor Proteins.Journal of molecular signaling · 2017Article
- LPP is a Src substrate required for invadopodia formation and efficient breast cancer lung metastasis.Nature communications · 2017Article
- Agonists and knockdown of estrogen receptor β differentially affect invasion of triple-negative breast cancer cells in vitro.BMC cancer · 2016Article
- Rictor/mTORC2 Drives Progression and Therapeutic Resistance of HER2-Amplified Breast Cancers.Cancer research · 2016Article
- Chordin-Like 1 Suppresses Bone Morphogenetic Protein 4-Induced Breast Cancer Cell Migration and Invasion.Molecular and cellular biology · 2016Article
- ShcA Protects against Epithelial-Mesenchymal Transition through Compartmentalized Inhibition of TGF-β-Induced Smad Activation.PLoS biology · 2015Article
- Transcriptomic characterization of fibrolamellar hepatocellular carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- p66Shc as a switch in bringing about contrasting responses in cell growth: implications on cell proliferation and apoptosis.Molecular cancer · 2015Review
- Granulocytic immune infiltrates are essential for the efficient formation of breast cancer liver metastases.Breast cancer research : BCR · 2015Article
- p66ShcA promotes breast cancer plasticity by inducing an epithelial-to-mesenchymal transition.Molecular and cellular biology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cooperation between the Neu/ErbB-2 and transforming growth factor beta (TGF-beta) signaling pathways enhances the invasive and metastatic capabilities of breast cancer cells; however, the underlying mechanisms mediating this synergy have yet to be fully explained. We demonstrate that TGF-beta induces the migration and invasion of mammary tumor explants expressing an activated Neu/ErbB-2 receptor, which requires signaling from autophosphorylation sites located in the C terminus. A systematic analysis of mammary tumor explants expressing Neu/ErbB-2 add-back receptors that couple to distinct signaling molecules has mapped the synergistic effect of TGF-beta-induced motility and invasion to signals emanating from tyrosine residues 1226/1227 and 1253 of Neu/ErbB-2. Given that the ShcA adaptor protein is known to interact with Neu/ErbB-2 through these residues, we investigated the importance of this signaling molecule in TGF-beta-induced cell motility and invasion. The reduction of ShcA expression rendered cells expressing activated Neu/ErbB-2, or add-back receptors signaling specifically through tyrosines 1226/1227 or 1253, unresponsive to TGF-beta-induced motility and invasion. In addition, a dominant-negative form of ShcA, lacking its three known tyrosine phosphorylation sites, completely abrogates the TGF-beta-induced migration and invasion of breast cancer cells expressing activated Neu/ErbB-2. Our results implicate signaling through the ShcA adaptor as a key component in the synergistic interaction between these pathways.
Indexed as
Identifiers
What OpenQuestion holds
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.