ArticleBritish journal of cancer1995
Activation of the E-cadherin/catenin complex in human MCF-7 breast cancer cells by all-trans-retinoic acid.
Article in British journal of cancer, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 76 citations in OpenAlex.
- UTX (KDM6A) promotes differentiation noncatalytically in somatic self-renewing epithelia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Retinoic Acids in the Treatment of Most Lethal Solid Cancers.Journal of clinical medicine · 2020Review
- Myoepithelial and luminal breast cancer cells exhibit different responses to all-trans retinoic acid.Cellular oncology (Dordrecht, Netherlands) · 2015Article
- RARβ2 hypermethylation is associated with poor recurrence-free survival in never-smokers with adenocarcinoma of the lung.Clinical epigenetics · 2015Article
- Cross-regulation of signaling pathways: an example of nuclear hormone receptors and the canonical Wnt pathway.Experimental cell research · 2010Review
- Wnt gene expression in human trabecular meshwork cells.Molecular vision · 2010Article
- Functional and molecular characterization of the epithelioid to round transition in human colorectal cancer LoVo cells.Oncogene · 2003Article
- Low-dose retinoic acid enhances in vitro invasiveness of human oral squamous-cell-carcinoma cell lines.British journal of cancer · 2001Article
- The alphaE-catenin gene (CTNNA1) acts as an invasion-suppressor gene in human colon cancer cells.Oncogene · 1999Article
- Somatic mutations of the beta-catenin gene are frequent in mouse and human hepatocellular carcinomas.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- All-trans-retinoic acid-dependent inhibition of E-cadherin-based cell adhesion with concomitant dephosphorylation of beta-catenin in metastatic human renal carcinoma cells.Japanese journal of cancer research : Gann · 1997Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
All-trans-retinoic acid (RA), like insulin-like growth factor I (IGF-I) and tamoxifen, inhibit invasion of human MCF-7/6 mammary cancer cells in vitro. For tamoxifen and for IGF-I, activation of the invasion-suppressor function of the E-cadherin/catenin complex was shown to be the most probable mechanism of the anti-invasive action. We did a series of experiments to determine whether the anti-invasive effect of RA also implicated the invasion-suppressor E-cadherin/catenin complex. Human MCF-7/6 mammary and HCT-8/R1 colon cancer cells, both with a dysfunctional E-cadherin/catenin complex, were treated with RA and the function of the complex was evaluated through Ca(2+)-dependent fast aggregation. Fast aggregation of both MCF-7/6 and HCT-8/R1 cells was induced by 1 microM RA. This effect was abolished by antibodies against E-cadherin. RA-induced fast aggregation was not sensitive to cycloheximide, tyrosine kinase inhibitors or antibodies against IGF-I or against the IGF-I receptor. RA did not stimulate IGF-I receptor phosphorylation or alter the E-cadherin/catenin complex, as evidenced by immunoprecipitation. RA up-regulates the function of the invasion-suppressor complex E-cadherin/catenin. Its action mechanism is different from that of IGF-I. RA may act as an anti-invasive agent with unique mechanisms of action.
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