ArticleMolecular and cellular biology2005
Immediate and delayed effects of E-cadherin inhibition on gene regulation and cell motility in human epidermoid carcinoma cells.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 48 citations in OpenAlex.
- Molecular mechanism of atractylon in the invasion and migration of hepatic cancer cells based on high‑throughput sequencing.Molecular medicine reports · 2022Article
- Gastric cancer with enhanced apical junction pathway has increased metastatic potential and worse clinical outcomes.American journal of cancer research · 2022Article
- Cadherin complexes recruit mRNAs and RISC to regulate epithelial cell signaling.The Journal of cell biology · 2017Article
- Diallyl disulfide suppresses epithelial-mesenchymal transition, invasion and proliferation by downregulation of LIMK1 in gastric cancer.Oncotarget · 2016Article
- A chemical energy approach of avascular tumor growth: multiscale modeling and qualitative results.SpringerPlus · 2015Article
- BAG3 regulates epithelial-mesenchymal transition and angiogenesis in human hepatocellular carcinoma.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- Article
- Activation of the PI3K/Akt/mTOR/p70S6K pathway is involved in S100A4-induced viability and migration in colorectal cancer cells.International journal of medical sciences · 2014Article
- Roles of transcriptional factor Snail and adhesion factor E-cadherin in clear cell renal cell carcinoma.Experimental and therapeutic medicine · 2013Article
- Asymmetric mode of Ca²⁺-S100A4 interaction with nonmuscle myosin IIA generates nanomolar affinity required for filament remodeling.Structure (London, England : 1993) · 2012Article
- Fra-1 controls motility of bladder cancer cells via transcriptional upregulation of the receptor tyrosine kinase AXL.Oncogene · 2012Article
- S100A4 mediated cell invasion and metastasis of esophageal squamous cell carcinoma via the regulation of MMP-2 and E-cadherin activity.Molecular biology reports · 2012Article
- ZEB2 mediates multiple pathways regulating cell proliferation, migration, invasion, and apoptosis in glioma.PloS one · 2012Article
- The expression of E-cadherin and cathepsin-D in normal oral mucosa, oral epithelial dysplasia and oral squamous cell carcinoma: A comparative analysis between immunohistochemistry and routine histopathology.Journal of oral and maxillofacial pathology : JOMFP · 2011Article
- Differential roles of STAT3 depending on the mechanism of STAT3 activation in gastric cancer cells.British journal of cancer · 2011Article
- Loss of function of e-cadherin in embryonic stem cells and the relevance to models of tumorigenesis.Journal of oncology · 2011Article
- ZEB1-responsive genes in non-small cell lung cancer.Cancer letters · 2011Article
- Three-dimensional multispecies nonlinear tumor growth-II: Tumor invasion and angiogenesis.Journal of theoretical biology · 2010Article
- Nonlinear modelling of cancer: bridging the gap between cells and tumours.Nonlinearity · 2010Article
- SIP1 protein protects cells from DNA damage-induced apoptosis and has independent prognostic value in bladder cancer.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The invasion suppressor protein, E-cadherin, plays a central role in epithelial cell-cell adhesion. Loss of E-cadherin expression or function in various tumors of epithelial origin is associated with a more invasive phenotype. In this study, by expressing a dominant-negative mutant of E-cadherin (Ec1WVM) in A431 cells, we demonstrated that specific inhibition of E-cadherin-dependent cell-cell adhesion led to the genetic reprogramming of tumor cells. In particular, prolonged inhibition of cell-cell adhesion activated expression of vimentin and repressed cytokeratins, suggesting that the effects of Ec1WVM can be classified as epithelial-mesenchymal transition. Both short-term and prolonged expression of Ec1WVM resulted in morphological transformation and increased cell migration though to different extents. Short-term expression of Ec1WVM up-regulated two AP-1 family members, c-jun and fra-1, but was insufficient to induce complete mesenchymal transition. AP-1 activity induced by the short-term expression of Ec1WVM was required for transcriptional up-regulation of AP-1 family members and down-regulation of two other Ec1WVM-responsive genes, S100A4 and igfbp-3. Using a dominant-negative mutant of c-Jun (TAM67) and RNA interference-mediated silencing of c-Jun and Fra-1, we demonstrated that AP-1 was required for cell motility stimulated by the expression of Ec1WVM. In contrast, Ec1WVM-mediated changes in cell morphology were AP-1-independent. Our data suggest that mesenchymal transition induced by prolonged functional inhibition of E-cadherin is a slow and gradual process. At the initial step of this process, Ec1WVM triggers a positive autoregulatory mechanism that increases AP-1 activity. Activated AP-1 in turn contributes to Ec1WVM-mediated effects on gene expression and tumor cell motility. These data provide novel insight into the tumor suppressor function of E-cadherin.
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.