Elaskalani O, Razak NBA, Falasca M, Metharom P. Epithelial-mesenchymal transition as a therapeutic target for overcoming chemoresistance in pancreatic cancer. World J Gastrointest Oncol 2017; 9(1): 37-41 [PMID: 28144398 DOI: 10.4251/wjgo.v9.i1.37]
Corresponding Author of This Article
Marco Falasca, PhD, Professor, Head of Metabolic Signalling Group, School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Kent Street, Bentley, Perth, Western Australia 6102, Australia. marco.falasca@curtin.edu.au
Research Domain of This Article
Oncology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastrointest Oncol. Jan 15, 2017; 9(1): 37-41 Published online Jan 15, 2017. doi: 10.4251/wjgo.v9.i1.37
Epithelial-mesenchymal transition as a therapeutic target for overcoming chemoresistance in pancreatic cancer
Omar Elaskalani, Norbaini Binti Abdol Razak, Marco Falasca, Pat Metharom
Omar Elaskalani, Norbaini Binti Abdol Razak, Pat Metharom, Platelet Research Laboratory, Curtin Health Innovation and Research Institute, Department of Health Sciences, Curtin University, Perth, Western Australia 6102, Australia
Norbaini Binti Abdol Razak, School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia 6102, Australia
Marco Falasca, Metabolic Signalling Group, School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia 6102, Australia
Author contributions: Falasca M initiated the manuscript concept; Elaskalani O researched and drafted the review; Elaskalani O and Razak NBA wrote the manuscript; Metharom P revised and contributed to the writing of the manuscript; Metharom P and Falasca M edited the manuscript; Falasca M approved the final version of the manuscript.
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Marco Falasca, PhD, Professor, Head of Metabolic Signalling Group, School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Kent Street, Bentley, Perth, Western Australia 6102, Australia. marco.falasca@curtin.edu.au
Telephone: +61-08-92669712
Received: September 14, 2016 Peer-review started: September 18, 2016 First decision: October 21, 2016 Revised: October 25, 2016 Accepted: November 21, 2016 Article in press: November 22, 2016 Published online: January 15, 2017
Abstract
Pancreatic cancer has one of the worst prognoses among all cancers due to the late manifestation of identifiable symptoms and high resistance to chemo- and radiation therapies. In recent years, a cancer development phase termed epithelial-mesenchymal transition (EMT) has gained increasing research focus. The process is implicated in tumour metastasis, and emerging evidence suggests EMT also contributes or induces chemoresistance in several cancers. Nevertheless, the applicability of therapeutic targeting of EMT faces many challenges. In this mini-review, we summarise the evidence supporting the role of EMT in pancreatic cancer progression, focusing particularly on its association with chemoresistance.
Core tip: This mini-review examines the role of epithelial-mesenchymal transition in the development of drug resistant pancreatic cancer and a possible use of this process as a drug target.
