ArticleOncogene2014
Soluble E-cadherin: a critical oncogene modulating receptor tyrosine kinases, MAPK and PI3K/Akt/mTOR signaling.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 97 citations in OpenAlex.
- Soluble E-cadherin-CXCL1-CXCR2 axis as a therapeutic vulnerability in inflammatory breast cancer brain metastasis.Neuro-oncology · 2026Article
- The feasible role of soluble E‑cadherin in spheroidogenesis of HCT116 colorectal cancer cells, a candidate biomarker for liquid biopsy.Oncology letters · 2025Article
- TMEM52B-derived peptides inhibit generation of soluble E-cadherin and EGFR activity to suppress colon cancer growth and early metastasis.Journal of translational medicine · 2025Article
- The diagnostic value of prostate health index combined with soluble e-cadherin for prostate cancer.Frontiers in endocrinology · 2025Article
- Active compounds of Caodoukou () inhibit the migration, invasion and metastasis of human pancreatic cancer cells by targeting phosphoinosmde-3-kinase/ protein kinase B/mammalian target of rapamycin pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- Regulation of Soluble E-Cadherin Signaling in Non-Small-Cell Lung Cancer Cells by Nicotine, BDNF, and β-Adrenergic Receptor Ligands.Biomedicines · 2023Article
- Increased soluble E‑cadherin of spheroid formation supplemented with fetal bovine serum in colorectal cancer cells.Oncology letters · 2023Article
- Article
- Dual role of E-cadherin in cancer cells.Tissue barriers · 2022Review
- MMP9: A Tough Target for Targeted Therapy for Cancer.Cancers · 2022Review
- Article
- Proteolytic Landscapes in Gastric Pathology and Cancerogenesis.International journal of molecular sciences · 2022Review
- TAGLN2-Regulated Trophoblast Migration, Invasion and Fusion are Impaired in Preeclampsia.Frontiers in cell and developmental biology · 2022Article
- Metformin for Cardiovascular Protection, Inflammatory Bowel Disease, Osteoporosis, Periodontitis, Polycystic Ovarian Syndrome, Neurodegeneration, Cancer, Inflammation and Senescence: What Is Next?ACS pharmacology & translational science · 2021Review
- Cellular senescence promotes cancer metastasis by enhancing soluble E-cadherin production.iScience · 2021Article
- Potential value of circulatory microRNA10b gene expression and its target E-cadherin as a prognostic and metastatic prediction marker for breast cancer.Journal of clinical laboratory analysis · 2021Article
- Long-term epilepsy-associated tumors: transcriptional signatures reflect clinical course.Scientific reports · 2020Article
- Application of proximity ligation assays to identify potential plasma biomarkers in oral cavity cancer patients: A case control study.Cancer biomarkers : section A of Disease markers · 2020Article
- Integrin Alpha V in Urine: A Novel Noninvasive Marker for Prostate Cancer Detection.Frontiers in oncology · 2020Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
E-cadherin, a cell-cell adhesion glycoprotein, is frequently downregulated with tumorigenic progression. The extracellular domain of E-cadherin is cleaved by proteases to generate a soluble ectodomain fragment, termed sEcad, which is elevated in the urine or serum of cancer patients. In this study, we explored the functional role of sEcad in the progression of skin squamous cell carcinomas (SCCs). We found that full-length E-cadherin expression was decreased and sEcad increased in human clinical tumor samples as well as in ultraviolet (UV)-induced SCCs in mice. Interestingly, sEcad associated with members of the human epidermal growth factor receptor (HER) and insulin-like growth factor-1 (IGF-1R) family of receptors in human and UV-induced mouse tumors. Moreover, in both E-cadherin-positive (E-cadherin(+)) and -negative (E-cadherin(-)) cells in vitro, sEcad activated downstream mitogen-activated protein (MAP) kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling and enhanced tumor growth, motility and invasion, the latter via activation of matrix metalloproteinase-2 (MMP-2) and MMP-9. To this end, HER, PI3K or MEK inhibitors suppressed sEcad's tumorigenic effects, including proliferation, migration and invasion. Taken together, our data suggest that sEcad contributes to skin carcinogenesis via association with the HER/IGF-1R-family of receptors and subsequent activation of the MAPK and PI3K/Akt/mTOR pathways, thereby implicating sEcad as a putative therapeutic target in cutaneous SCCs.
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.