ArticleScientific reports2015
The N-cadherin cytoplasmic domain confers anchorage-independent growth and the loss of contact inhibition.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Migrating mesoderm cells self-organize into a dynamic meshwork structure during chick gastrulation.eLife · 2025Article
- The Role of Mechanotransduction in Contact Inhibition of Locomotion and Proliferation.International journal of molecular sciences · 2024Review
- Capsaicinoids and Their Effects on Cancer: The "Double-Edged Sword" Postulate from the Molecular Scale.Cells · 2023Review
- A CaMolecular cancer research : MCR · 2019Article
- A central role for cadherin signaling in cancer.Experimental cell research · 2017Review
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Authors and funding
1 author at 1 institution in 1 country.
Funding
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Abstract
Tumor growth is characterized by anchorage independence and the loss of contact inhibition. Previously, we showed that either a red fluorescent protein (DsRed)-tagged N-cadherin or E-cadherin cytoplasmic domain (DNCT or DECT) could function as a dominant negative inhibitor by blocking the cell surface localization of endogenous E-cadherin and inducing cell dissociation. Here, we show that expression of DNCT abrogated contact inhibition of proliferation and conferred anchorage-independent growth. DNCT expression induced the relocation of the tumor suppressor Merlin from the cell surface to intracellular compartments. Although DNCT expression induced redistribution of TAZ from the cytoplasm to the nucleus, YAP/TAZ signaling was not activated. An E-cadherin-α-catenin chimera that functions as a β-catenin-independent cell adhesion molecule restored contact inhibition and anchorage-dependency of growth. Addition of the SV40 large T antigen nuclear localization signal reversed the effects of DNCT expression, indicating that DNCT functioned outside of the nucleus.
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