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Grelet et al. J Cancer Metastasis Treat 2019;5:16 Journal of Cancer
DOI: 10.20517/2394-4722.2018.85 Metastasis and Treatment

Review Open Access

hnRNP E1 at the crossroads of translational
regulation of epithelial-mesenchymal transition

Simon Grelet , Philip H. Howe 1,2
1,2

1 Hollings Cancer Center, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
2 Department of Biochemistry, Medical University of South Carolina, Charleston, South Carolina 29425, USA.

Correspondence to: Dr. Simon Grelet and Prof. Philip H. Howe, Department of Biochemistry, Medical University of South
Carolina, Charleston, South Carolina 29425, USA. E-mail: grelet@musc.edu; howep@musc.edu

How to cite this article: Grelet S, Howe PH. hnRNP E1 at the crossroads of translational regulation of epithelial-mesenchymal
transition. J Cancer Metastasis Treat 2019;5:16. http://dx.doi.org/10.20517/2394-4722.2018.85

Received: 1 Dec 2018 First Decision: 30 Dec 2018 Revised: 10 Jan 2019 Accepted: 22 Jan 2019 Published: 11 Mar 2019

Science Editor: William P. Schiemann Copy Editor: Cai-Hong Wang Production Editor: Huan-Liang Wu

Abstract
The epithelial-mesenchymal transition (EMT), in which cells undergo a switch from a polarized, epithelial
phenotype to a highly motile fibroblastic or mesenchymal phenotype is fundamental during embryonic
development and can be reactivated in a variety of diseases including cancer. Spatio-temporally-regulated
mechanisms are constantly orchestrated to allow cells to adapt to their constantly changing environments
when disseminating to distant organs. Although numerous transcriptional regulatory factors are currently well-
characterized, the post-transcriptional control of EMT requires continued investigation. The hnRNP E1 protein
displays a major role in the control of tumor cell plasticity by regulating the translatome through multiple non-
redundant mechanisms, and this role is exemplified when E1 is absent. hnRNP E1 binding to RNA molecules leads
to direct or indirect translational regulation of specific sets of proteins: (1) hnRNP E1 binding to specific targets has
a direct role in translation by preventing elongation of translation; (2) hnRNP E1-dependent alternative splicing
can prevent the generation of a competing long non-coding RNA that acts as a decoy for microRNAs (miRNAs)
involved in translational inhibition of EMT master regulators; (3) hnRNP E1 binding to the 3’ untranslated region of
transcripts can also positively regulate the stability of certain mRNAs to improve their translation. Globally, hnRNP
E1 appears to control proteome reprogramming during cell plasticity, either by direct or indirect regulation of
protein translation.

Keywords: Breast cancer, tumor progression, epithelial-mesenchymal transition, cancer stem cells, transforming
growth factor-β, translation, hnRNP E1, PCBP1

© The Author(s) 2019. Open Access This article is licensed under a Creative Commons Attribution 4.0
International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
and indicate if changes were made.

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