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The human NANOS3 gene contributes to lung tumour invasion by inducing epithelial–mesenchymal transition
Author(s) -
Grelet Simon,
Andries Vanessa,
Polette Myriam,
Gilles Christine,
Staes Katrien,
Martin AnnePascaline,
Kileztky Claire,
Terryn Christine,
Dalstein Véronique,
Cheng ChunWen,
Shen ChenYang,
Birembaut Philippe,
Van Roy Frans,
NawrockiRaby Béatrice
Publication year - 2015
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.4549
Subject(s) - vimentin , gene silencing , epithelial–mesenchymal transition , biology , cancer research , epigenetics , microrna , transition (genetics) , microbiology and biotechnology , gene , immunohistochemistry , immunology , genetics
We have explored the role of the human NANOS3 gene in lung tumour progression. We show that NANOS3 is over‐expressed by invasive lung cancer cells and is a prognostic marker for non‐small cell lung carcinomas ( NSCLCs ). NANOS3 gene expression is restricted in testis and brain and is regulated by epigenetic events. It is up‐regulated in cultured cells undergoing epithelial − mesenchymal transition ( EMT ). NANOS3 over‐expression in human NSCLC cell lines enhances their invasiveness by up‐regulating EMT , whereas its silencing induces mesenchymal − epithelial transition. NANOS3 represses E‐cadherin at the transcriptional level and up‐regulates vimentin post‐transcriptionally. Also, we show that NANOS3 binds mRNAs encoding vimentin and regulates the length of their poly(A) tail. Finally, NANOS3 can also protect vimentin mRNA from microRNA ‐mediated repression. We thus demonstrate a role for NANOS3 in the acquisition of invasiveness by human lung tumour cells and propose a new mechanism of post‐transcriptional regulation of EMT . Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.