ArticleHuman molecular genetics2015
E-cadherin-defective gastric cancer cells depend on Laminin to survive and invade.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Loss of L1CAM from gastric epithelial cells and extracellular vesicles promotes Helicobacter pylori-driven cancer progression and invasiveness.Cell communication and signaling : CCS · 2026Article
- Article
- Clinical importance of E-cadherin deficiency in resectable gastric cancer: A nested case-control study.Oncology letters · 2025Article
- The ECM and tissue architecture are major determinants of early invasion mediated by E-cadherin dysfunction.Communications biology · 2023Article
- Engineering the Interactions of Classical Cadherin Cell-Cell Adhesion Proteins.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Decision-making and regret in patients with germlineJournal of medical genetics · 2023Article
- Molecular mechanism for strengthening E-cadherin adhesion using a monoclonal antibody.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- circRNA: A New Biomarker and Therapeutic Target for Esophageal Cancer.Biomedicines · 2022Review
- Investigating the mechanisms of peritoneal metastasis in gastric adenocarcinoma using a novel ex vivo peritoneal explant model.Scientific reports · 2022Article
- Differential Impacts on Tensional Homeostasis of Gastric Cancer Cells Due to Distinct Domain Variants of E-Cadherin.Cancers · 2022Article
- Integrin β1 orchestrates the abnormal cell-matrix attachment and invasive behaviour of E-cadherin dysfunctional cells.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022Article
- Circular RNA hsa_circ_0000277 sequesters miR-4766-5p to upregulate LAMA1 and promote esophageal carcinoma progression.Cell death & disease · 2021Article
- Review
- Clinical spectrum and pleiotropic nature ofJournal of medical genetics · 2019Review
- Multicellular Human Gastric-Cancer Spheroids Mimic the Glycosylation Phenotype of Gastric Carcinomas.Molecules (Basel, Switzerland) · 2018Article
- The polymorphism in miR-25 attenuated the oncogenic function in gastric cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Epithelial-cadherin (Ecad) deregulation affects cell-cell adhesion and results in increased invasiveness of distinct human carcinomas. In gastric cancer, loss of Ecad expression is a common event and is associated with disease aggressiveness and poor prognosis. However, the molecular mechanisms underlying the invasive process associated to Ecad dysfunction are far from understood. We hypothesized that deregulation of cell-matrix interactions could play an important role during this process. Thus, we focussed on LM-332, which is a major matrix component, and in Ecad/LM-332 crosstalk in the process of Ecad-dependent invasion. To verify whether matrix deregulation was triggered by Ecad loss, we used the Drosophila model. To dissect the key molecules involved and unveil their functional significance, we used gastric cancer cell lines. The relevance of this relationship was then confirmed in human primary tumours. In vivo, Ecad knockdown induced apoptosis; nonetheless, at the invasive front, cells ectopically expressed Laminin A and βPS integrin. In vitro, we demonstrated that, in two different gastric cancer cell models, Ecad-defective cells overexpressed Laminin γ2 (LM-γ2), β1 and β4 integrin, when compared with Ecad-competent ones. We showed that LM-γ2 silencing impaired invasion and enhanced cell death, most likely via pSrc and pAkt reduction, and JNK activation. In human gastric carcinomas, we found a concomitant decrease in Ecad and increase in LM-γ2. This is the first evidence that ectopic Laminin expression depends on Ecad loss and allows Ecad-dysfunctional cells to survive and invade. This opens new avenues for using LM-γ2 signalling regulators as molecular targets to impair gastric cancer progression.
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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.