The DOI matches its Crossref record; 109 of the 109 references it cites were found in a registry or an index.
E-cadherin–integrin crosstalk in cancer invasion and metastasis
Abstract
Summary: E-cadherin is a single-pass transmembrane protein that mediates homophilic cell–cell interactions. Tumour progression is often associated with the loss of E-cadherin function and the transition to a more motile and invasive phenotype. This requires the coordinated regulation of both E-cadherin-mediated cell–cell adhesions and integrin-mediated adhesions that contact the surrounding extracellular matrix (ECM). Regulation of both types of adhesion is dynamic as cells respond to external cues from the tumour microenvironment that regulate polarity, directional migration and invasion. Here, we review the mechanisms by which tumour cells control the cross-regulation between dynamic E-cadherin-mediated cell–cell adhesions and integrin-mediated cell–matrix contacts, which govern the invasive and metastatic potential of tumours. In particular, we will discuss the role of the adhesion-linked kinases Src, focal adhesion kinase (FAK) and integrin-linked kinase (ILK), and the Rho family of GTPases.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Hallmarks of Cancer: The Next Generation
Hanahan, D., & Weinberg, R. A. (2011) · Cell · doi:10.1016/j.cell.2011.02.013 · Cited by 66,590
The basics of epithelial-mesenchymal transition
Kalluri, R., & Weinberg, R. A. (2009) · Journal of Clinical Investigation · doi:10.1172/jci39104 · Cited by 10,196
Hynes (2002) · doi:10.1016/s0092-8674(02)00971-6 · Cited by 8,606
Massagué, J. (1998) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.67.1.753 · Cited by 7,556
Epithelial–mesenchymal transitions in tumour progression
Thiery, J. P. (2002) · Nature Reviews Cancer · doi:10.1038/nrc822 · Cited by 6,628
Tumor Metastasis: Molecular Insights and Evolving Paradigms
Valastyan, S., & Weinberg, R. A. (2011) · Cell · doi:10.1016/j.cell.2011.09.024 · Cited by 4,011
RHO GTPASES: Biochemistry and Biology
Jaffe, A. B., & Hall, A. (2005) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev.cellbio.21.020604.150721 · Cited by 3,009
Collective cell migration in morphogenesis, regeneration and cancer
Friedl, P., & Gilmour, D. (2009) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2720 · Cited by 2,712
Cell adhesion: integrating cytoskeletal dynamics and cellular tension
Parsons, J. T., Horwitz, A. R., & Schwartz, M. A. (2010) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2957 · Cited by 1,988
Cancer Invasion and the Microenvironment: Plasticity and Reciprocity
Friedl, P., & Alexander, S. (2011) · Cell · doi:10.1016/j.cell.2011.11.016 · Cited by 1,940
Cited by
Every step of the way: integrins in cancer progression and metastasis
Hamidi, H., & Ivaska, J. (2018) · Nature Reviews Cancer · doi:10.1038/s41568-018-0038-z · Cited by 1,493
FAK in cancer: mechanistic findings and clinical applications
Sulzmaier, F. J., Jean, C., & Schlaepfer, D. D. (2014) · Nature Reviews Cancer · doi:10.1038/nrc3792 · Cited by 1,381
3D scaffolds in breast cancer research
Rijal, G., & Li, W. (2016) · Biomaterials · doi:10.1016/j.biomaterials.2015.12.016 · Cited by 169
Focal adhesion kinase: from biological functions to therapeutic strategies
Tan, X., Yan, Y., Song, B., Zhu, S., Mei, Q., & Wu, K. (2023) · Experimental Hematology & Oncology · doi:10.1186/s40164-023-00446-7 · Cited by 158
The Roles of MicroRNAs in Breast Cancer
Takahashi, R.-U., Miyazaki, H., & Ochiya, T. (2015) · Cancers · doi:10.3390/cancers7020598 · Cited by 116
Metadata
- Authors
- Canel, M., Serrels, A., Frame, M. C., & Brunton, V. G.
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- Published
- 2013-01-15
- Volume
- 126
- Issue
- 2
- Pages
- 393-401
- ISSN
- 0021-9533 (ISSN-L)
- 1477-9137
- OpenAlex
- W2002603913
- Cited by
- 623
- References
- 109
- FWCI
- 48.15
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: E-cadherin–integrin crosstalk in cancer invasion and metastasis. https://app.cochat.ai/papers/10.1242/jcs.100115
- The paper
- Canel, M., Serrels, A., Frame, M. C., & Brunton, V. G. (2013). E-cadherin–integrin crosstalk in cancer invasion and metastasis. Journal of Cell Science. https://doi.org/10.1242/jcs.100115
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.