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Published in: Journal of Cancer Research and Clinical Oncology 10/2017

01-10-2017 | Review – Cancer Research

Mitochondrial DNA variants in colorectal carcinogenesis: Drivers or passengers?

Authors: Edoardo Errichiello, Tiziana Venesio

Published in: Journal of Cancer Research and Clinical Oncology | Issue 10/2017

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Abstract

Introduction

Mitochondrial DNA alterations have widely been reported in many age-related degenerative diseases and tumors, including colorectal cancer. In the past few years, the discovery of inter-genomic crosstalk between nucleus and mitochondria has reinforced the role of mitochondrial DNA variants in perturbing this essential signaling pathway and thus indirectly targeting nuclear genes involved in tumorigenic and invasive phenotype.

Findings

Mitochondrial dysfunction is currently considered a crucial hallmark of carcinogenesis as well as a promising target for anticancer therapy. Mitochondrial DNA alterations include point mutations, deletions, inversions, and copy number variations, but numerous studies investigating their pathogenic role in cancer have provided inconsistent evidence. Furthermore, the biological impact of mitochondrial DNA variants may vary tremendously, depending on the proportion of mutant DNA molecules carried by the neoplastic cells (heteroplasmy).

Conclusions

In this review, we discuss the role of different type of mitochondrial DNA alterations in colorectal carcinogenesis and, in particular, we revisit the issue of whether they may be considered as causative driver or simply genuine passenger events. The advent of high-throughput techniques as well as the development of genetic and pharmaceutical interventions for the treatment of mitochondrial dysfunction in colorectal cancer are also explored.
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Metadata
Title
Mitochondrial DNA variants in colorectal carcinogenesis: Drivers or passengers?
Authors
Edoardo Errichiello
Tiziana Venesio
Publication date
01-10-2017
Publisher
Springer Berlin Heidelberg
Published in
Journal of Cancer Research and Clinical Oncology / Issue 10/2017
Print ISSN: 0171-5216
Electronic ISSN: 1432-1335
DOI
https://doi.org/10.1007/s00432-017-2418-2

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