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An alternative way for epithelial-to-mesenchymal transition in colorectal cancer via EIF5A2?
  1. Frank T Kolligs
  1. Correspondence to Dr Frank T Kolligs, Department of Medicine II, University of Munich, Marchioninistr. 15, 81377 Munich, Germany; fkolligs{at}med.uni-muenchen.de

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Epithelial-to-mesenchymal transition (EMT) is a reversible programme which allows the transition between the epithelial and the mesenchymal phenotype in embryonic development, the differentiation of tissues and organs and tissue repair.1 A direct link between EMT and epithelial stem cell properties has been demonstrated.2 Aberrant activation of EMT is a trigger for organ fibrosis and the progression and metastasis of epithelial cancers.1 In colorectal cancer, EMT occurs at the invasive front of the tumour and results in the generation of single migratory cells which have lost expression of the adherens junction protein E-cadherin and have gained expression of both vimentin and fibronectin at the same time. Additionally, these cells show activation of the Wnt signalling pathway.3 At the histopathological level, tumour budding—the detachment of tumour cells from the main tumour—has been described to be closely related to EMT and has been found to be an adverse prognostic factor.4 Depending on tissue and cell type, EMT is activated by several key pathways, including TGF (transforming growth factor) β, Notch and FGF (fibroblast growth factor) signalling which converge in the stimulation of a group of transcription factors repressing epithelial gene expression.5

The gene EIF5A2 encodes the eukaryotic initiation factor 5A2 and is located on chromosome 3q26, a region frequently amplified in several tumours.6 EIF5A2 has been shown to induce anchorage-independent growth and xenograft tumour growth of ovarian …

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