ArticleMolecular carcinogenesis2014
Soluble-E-cadherin activates HER and IAP family members in HER2+ and TNBC human breast cancers.
Article in Molecular carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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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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.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Soluble E-cadherin-CXCL1-CXCR2 axis as a therapeutic vulnerability in inflammatory breast cancer brain metastasis.Neuro-oncology · 2026Article
- Application of antibody-drug conjugates in locally advanced or metastatic urothelial carcinoma: mechanisms, treatment-related adverse events, and management strategies.Frontiers in pharmacology · 2026Review
- Molecular targets and therapies associated with poor prognosis of triple‑negative breast cancer (Review).International journal of oncology · 2025Review
- Clinical utility of quantitative ultrasonography parameters combined with serum cancer antigen 15‑3, human epidermal growth factor receptor 2 and soluble E‑cadherin in diagnosing mass‑type breast cancer.Oncology letters · 2025Article
- Regulation of Soluble E-Cadherin Signaling in Non-Small-Cell Lung Cancer Cells by Nicotine, BDNF, and β-Adrenergic Receptor Ligands.Biomedicines · 2023Article
- Article
- The Cross-Talk Between EGFR and E-Cadherin.Frontiers in cell and developmental biology · 2021Review
- E-cadherin-Fc chimera protein matrix enhances cancer stem-like properties and induces mesenchymal features in colon cancer cells.Cancer science · 2019Article
- Targeting the Temporal Dynamics of Hypoxia-Induced Tumor-Secreted Factors Halts Tumor Migration.Cancer research · 2019Article
- Cut loose and run: The complex role of ADAM proteases during neural crest cell development.Genesis (New York, N.Y. : 2000) · 2018Review
- Cadherins function during the collective cell migration of Xenopus Cranial Neural Crest cells: revisiting the role of E-cadherin.Mechanisms of development · 2017Review
- Article
- Expression of human endogenous retrovirus-K is strongly associated with the basal-like breast cancer phenotype.Scientific reports · 2017Article
- The ectodomain of cadherin-11 binds to erbB2 and stimulates Akt phosphorylation to promote cranial neural crest cell migration.PloS one · 2017Article
- Roles of RUNX in Hippo Pathway Signaling.Advances in experimental medicine and biology · 2017Review
- Prognostic value of HER2 status in bladder transitional cell carcinoma revealed by both IHC and BDISH techniques.BMC cancer · 2016Article
- Carcinoma cells induce lumen filling and EMT in epithelial cells through soluble E-cadherin-mediated activation of EGFR.Journal of cell science · 2015Article
- RUNX2 and TAZ-dependent signaling pathways regulate soluble E-Cadherin levels and tumorsphere formation in breast cancer cells.Oncotarget · 2015Article
- Inflammation-induced desmoglein-2 ectodomain shedding compromises the mucosal barrier.Molecular biology of the cell · 2015Article
- Protein arginine methyltransferase 7 promotes breast cancer cell invasion through the induction of MMP9 expression.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Recent literature suggests that sEcad exerts pro-oncogenic effects, possibly acting as a ligand for the human epidermal growth factor family. Here we show that sEcad is a novel candidate protein for drug targeting since it is increased in human and mouse HER2-positive (HER2+) breast tumors, MMTV-PyMT bodily fluids and human cell culture systems. Mechanistically, we show that endogenous sEcad, and to a lesser extent membrane-bound E-cadherin, associates with HER1, HER2, and HER3 in human and MMTV-PyMT mouse HER2+ tumors and with HER1 in triple negative breast cancer (TNBC) specimens. Furthermore, addition of exogenous recombinant human E-cadherin/Fc chimeric protein (rhEcad/Fc; sEcad) to HER2+ MCF-7, SKBR3, and HER2-negative MDA-MB-231 TNBC cells, resulted in sEcad-HER receptor family interactions, activation of HER1-4 and downstream pro-survival signaling, including the MAPK-PI3K/Akt/mTOR pathways and IAP family members. Lastly, we demonstrate that sEcad exerts pro-oncogenic effects via HER signaling, and acts additively with the HER ligand EGF to promote HER2+ breast cancer proliferation and migration, as well as TNBC invasion. Because sEcad associates and activates many of the oncogenic pathways that tumors utilize for growth and survival and serum levels in patients correlates with clinical response, suggests that targeted therapy against sEcad in combination with other therapies may potentially offer a novel therapeutic strategy for the treatment of breast cancers.
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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.