MiR-675-5p supports hypoxia induced epithelial to mesenchymal transition in colon cancer cells

Viviana Costa; Alessia Lo Dico; Aroldo Rizzo; Francesca Rajata; Marco Tripodi; Riccardo Alessandro; Alice Conigliaro

doi:10.18632/oncotarget.14464

Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. The term was introduced in the inaugural Editorial, Introducing Oncotarget.

As of January 1, 2022, Oncotarget has shifted to a continuous publishing model. Papers will now be published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Subscribe to receive alerts once a paper has been published by Oncotarget.

Impact Journals, LLC is the publisher of Oncotarget: www.impactjournals.com.

Impact Journals is a member of the Wellcome Trust List of Compliant Publishers.

Impact Journals is a member of the Society for Scholarly Publishing.

On December 23, 2022, Oncotarget server experienced a DDoS attack. As a result, Oncotarget site was inaccessible for a few hours. Oncotarget team swiftly dealt with the situation and took it under control. This malicious action will be reported to the FBI.

Research Papers:

MiR-675-5p supports hypoxia induced epithelial to mesenchymal transition in colon cancer cells

Viviana Costa, Alessia Lo Dico, Aroldo Rizzo, Francesca Rajata, Marco Tripodi, Riccardo Alessandro and Alice Conigliaro _

PDF | HTML | Supplementary Files | How to cite

Oncotarget. 2017; 8:24292-24302. https://doi.org/10.18632/oncotarget.14464

Metrics: PDF 2941 views | HTML 3414 views | ?

Abstract

Viviana Costa1,*, Alessia Lo Dico2,*, Aroldo Rizzo3, Francesca Rajata3, Marco Tripodi4,5, Riccardo Alessandro6,7,*, Alice Conigliaro4,*

1Innovative Technological Platforms for Tissue Engineering, Theranostic and Oncology, Rizzoli Orthopedic Institute, Palermo, Italy

2Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Milano, Italy

3Unità Operativa di Anatomia Patologica, Azienda Ospedaliera Ospedali Riuniti “Villa Sofia-Cervello”, Palermo, Italy

4Dipartimento di Biotecnologie Cellulari ed Ematologia, Sapienza University of Rome, Rome, Italy

5National Institute for Infectious Diseases L. Spallanzani, IRCCS, Rome, Italy

6Dipartimento di Biopatologia e Biotecnologie Mediche, University of Palermo, Palermo, Italy

7Institute of Biomedicine and Molecular Immunology (IBIM), National Research Council of Italy, Palermo, Italy

*These authors contributed equally to this work

Correspondence to:

Alice Conigliaro, email: [email protected]

Riccardo Alessandro, email: [email protected]

Keywords: miRNA675, CRC, EMT, metastasis, hypoxia

Received: November 16, 2016 Accepted: December 27, 2016 Published: January 03, 2017

ABSTRACT

The survival rates in colon cancer patients are inversely proportional to the number of lymph node metastases. The hypoxia-induced Epithelial to Mesenchymal Transition (EMT), driven by HIF1α, is known to be involved in cancer progression and metastasis. Recently, we have reported that miR-675-5p promotes glioma growth by stabilizing HIF1α; here, by use of the syngeneic cell lines we investigated the role of the miR-675-5p in colon cancer metastasis.

Our results show that miR-675-5p, over expressed in metastatic colon cancer cells, participates to tumour progression by regulating HIF1α induced EMT. MiR-675-5p increases Snail transcription by a dual strategy: i) stabilizing the activity of the transcription factor HIF1α and ii) and inhibiting Snail’s repressor DDB2 (Damage specific DNA Binding protein 2).

Moreover, transcriptional analyses on specimens from colon cancer patients confirmed, in vivo, the correlation between miR-675-5p over-expression and metastasis, thus identifying miR-675-5p as a new marker for colon cancer progression and therefore a putative target for therapeutic strategies.

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 14464

Publication Alerts

Research Papers:

MiR-675-5p supports hypoxia induced epithelial to mesenchymal transition in colon cancer cells

Abstract