Distinct E-cadherin-based complexes regulate cell behaviour through miRNA processing or Src and p120 catenin activity View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-09

AUTHORS

Antonis Kourtidis, Siu P Ngok, Pamela Pulimeno, Ryan W Feathers, Lomeli R Carpio, Tiffany R Baker, Jennifer M Carr, Irene K Yan, Sahra Borges, Edith A Perez, Peter Storz, John A Copland, Tushar Patel, E Aubrey Thompson, Sandra Citi, Panos Z Anastasiadis

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. More... »

PAGES

1145-1157

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncb3227

DOI

http://dx.doi.org/10.1038/ncb3227

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1011165680

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26302406


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