ArticleNature cell biology2015
Distinct E-cadherin-based complexes regulate cell behaviour through miRNA processing or Src and p120 catenin activity.
Article in Nature cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
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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.
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Who cites it
62 citing papers in PubMed, 109 citations in OpenAlex.
- Multiomics analysis reveals dermokine as a regulator of keratinocyte differentiation and adhesion.JCI insight · 2026Article
- PIWIL2 downregulation in colon cancer promotes transposon activity and pro-tumorigenic phenotypes.Biology open · 2025Article
- The subcellular topology of the RNAi machinery is multifaceted and reveals adherens junctions as an epithelial hub.Scientific reports · 2025Article
- The epithelial adherens junction component PLEKHA7 regulates ECM remodeling and cell behavior through miRNA-mediated regulation of MMP1 and LOX.bioRxiv : the preprint server for biology · 2024Article
- Article
- Critical roles of adherens junctions in diseases of the oral mucosa.Tissue barriers · 2023Article
- The hTERT-p50 homodimer inhibits PLEKHA7 expression to promote gastric cancer invasion and metastasis.Oncogene · 2023Article
- Cadherins and catenins in cancer: connecting cancer pathways and tumor microenvironment.Frontiers in cell and developmental biology · 2023Review
- ECM Substrates Impact RNAi Localization at Adherens Junctions of Colon Epithelial Cells.Cells · 2022Article
- Dual role of E-cadherin in cancer cells.Tissue barriers · 2022Review
- Bioengineered PLEKHA7 nanodelivery regularly induces behavior alteration and growth retardation of acute myeloid leukemia.Biomaterials and biosystems · 2022Article
- Article
- Origin and Evolution of the Multifaceted Adherens Junction Component Plekha7.Frontiers in cell and developmental biology · 2022Article
- Profiling of RNA-binding Proteins Interacting With Glucagon and Adipokinetic Hormone mRNAs.Journal of lipid and atherosclerosis · 2022Article
- PLEKHA7 signaling is necessary for the growth of mutant KRAS driven colorectal cancer.Experimental cell research · 2021Article
- Structural basis for the association of PLEKHA7 with membrane-embedded phosphatidylinositol lipids.Structure (London, England : 1993) · 2021Article
- LNCcation: lncRNA localization and function.The Journal of cell biology · 2021Review
- PLEKHA7, an Apical Adherens Junction Protein, Suppresses Inflammatory Breast Cancer in the Context of High E-Cadherin and p120-Catenin Expression.International journal of molecular sciences · 2021Article
- WW, PH and C-Terminal Domains Cooperate to Direct the Subcellular Localizations of PLEKHA5, PLEKHA6 and PLEKHA7.Frontiers in cell and developmental biology · 2021Article
- E-cadherin Interacts With Posttranslationally-Modified AGO2 to Enhance miRISC Activity.Frontiers in cell and developmental biology · 2021Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
E-cadherin and p120 catenin (p120) are essential for epithelial homeostasis, but can also exert pro-tumorigenic activities. Here, we resolve this apparent paradox by identifying two spatially and functionally distinct junctional complexes in non-transformed polarized epithelial cells: one growth suppressing at the apical zonula adherens (ZA), defined by the p120 partner PLEKHA7 and a non-nuclear subset of the core microprocessor components DROSHA and DGCR8, and one growth promoting at basolateral areas of cell-cell contact containing tyrosine-phosphorylated p120 and active Src. Recruitment of DROSHA and DGCR8 to the ZA is PLEKHA7 dependent. The PLEKHA7-microprocessor complex co-precipitates with primary microRNAs (pri-miRNAs) and possesses pri-miRNA processing activity. PLEKHA7 regulates the levels of select miRNAs, in particular processing of miR-30b, to suppress expression of cell transforming markers promoted by the basolateral complex, including SNAI1, MYC and CCND1. Our work identifies a mechanism through which adhesion complexes regulate cellular behaviour and reveals their surprising association with the microprocessor.
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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.