Oncotarget

Reviews:

Distinct functions of dynamin isoforms in tumorigenesis and their potential as therapeutic targets in cancer

Jianghui Meng _

PDF  |  HTML  |  How to cite  |  Order a Reprint

Oncotarget. 2017; 8:41701-41716. https://doi.org/10.18632/oncotarget.16678

Metrics: PDF 636 views  |   HTML 1076 views  |   ?  


Abstract

Jianghui Meng1,2

1 Charles Institute of Dermatology, School of Medicine and Medical Sciences, University College Dublin, Belfield, Dublin, Ireland

2 International Centre for Neurotherapeutics, Dublin City University, Glasnevin, Dublin, Ireland

Correspondence to:

Jianghui Meng, email:

email:

Keywords: endocytosis, tumor, cancer target, clathrin, amphiphysin

Received: September 28, 2016 Accepted: March 09, 2017 Published: March 29, 2017

Abstract

Dynamins and their related proteins participate in the regulation of neurotransmission, antigen presentation, receptor internalization, growth factor signalling, nutrient uptake, and pathogen infection. Recently, emerging findings have shown dynamin proteins can also contribute to the genesis of cancer. This up-to-date review herein focuses on the functionality of dynamin in cancer development. Dynamin 1 and 2 both enhance cancer cell proliferation, tumor invasion and metastasis, whereas dynamin 3 has tumor suppression role. Antisense RNAs encoded on the DNA strand opposite a dynamin gene regulate the function of dynamin, and manipulate oncogenes and tumor suppressor genes. Certain dynamin-related proteins are also upregulated in distinct cancer conditions, resulting in apoptotic resistance, cell migration and poor prognosis. Altogether, dynamins are potential biomarkers as well as representing promising novel therapeutic targets for cancer treatment. This study also summarizes the current available dynamin-targeted therapeutics and suggests the potential strategy based on signalling pathways involved, providing important information to aid the future development of novel cancer therapeutics by targeting these dynamin family members.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 16678