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Loss of miR ‐101 expression promotes Wnt/ β ‐catenin signalling pathway activation and malignancy in colon cancer cells
Author(s) -
Strillacci Antonio,
Valerii Maria Chiara,
Sansone Pasquale,
Caggiano Cinzia,
Sgromo Annamaria,
Vittori Laura,
Fiorentino Michelangelo,
Poggioli Gilberto,
Rizzello Fernando,
Campieri Massimo,
Spisni Enzo
Publication year - 2013
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.4097
Subject(s) - colorectal cancer , wnt signaling pathway , cancer research , microrna , malignancy , cancer , suppressor , epithelial–mesenchymal transition , biology , biomarker , gene knockdown , signal transduction , metastasis , medicine , pathology , microbiology and biotechnology , cell culture , gene , genetics
Colorectal cancer ( CRC ) is the second leading cause of cancer‐related mortality in Western countries. Although the aberrant expression of several microRNAs ( oncomiRs ) is associated with CRC progression, the molecular mechanisms of this phenomenon are still under investigation. Here we show that miR ‐101 expression is differentially impaired in CRC specimens, depending on tumour grade. miR ‐101 re‐expression suppresses cell growth in 3D , hypoxic survival and invasive potential in CRC cells showing low levels of miR ‐101 . Additionally, we provide molecular evidence of a bidirectional regulatory mechanism between miR ‐101 expression and important CRC pro‐malignant features, such as inflammation, activation of the Wnt/ β ‐catenin signalling pathway and epithelial–mesenchymal transition ( EMT ). We then propose that up‐regulated miR ‐101 may function as a tumour suppressor in CRC and that its pharmacological restoration might hamper the aggressive behaviour of CRC in vivo . MiR ‐101 expression may also represent a cancer biomarker for CRC diagnosis and prognosis. Copyright © 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.