Open Access
International Journal of Molecular Sciences, volume 19, issue 7, pages 2076
Mitochondrial Dysfunctions in Type I Endometrial Carcinoma: Exploring Their Role in Oncogenesis and Tumor Progression
Clara Musicco
1
,
Gennaro Cormio
2, 3
,
Vito Pesce
4
,
Vera Loizzi
2
,
Ettore Cicinelli
2
,
Leonardo Resta
5
,
Girolamo Ranieri
6
,
Antonella Cormio
4
1
CNR–Institute of Biomembranes, Bioenergetics and Molecular Biotechnologies (IBIOM), Via Amendola 165/A, 70126 Bari, Italy
|
3
Gynecologic Oncology Unit, National Cancer Center “Giovanni Paolo II”, Viale Orazio Flacco, 65, 70124 Bari, Italy
|
6
Interventional Radiology Unit with Integrated Section of Translational Medical Oncology, National Cancer Centre ″Giovanni Paolo II″, Viale Orazio Flacco, 65, 70124 Bari, Italy
|
Publication type: Journal Article
Publication date: 2018-07-17
scimago Q1
SJR: 1.179
CiteScore: 8.1
Impact factor: 4.9
ISSN: 16616596, 14220067
PubMed ID:
30018222
Catalysis
Organic Chemistry
Inorganic Chemistry
Physical and Theoretical Chemistry
Computer Science Applications
Spectroscopy
Molecular Biology
General Medicine
Abstract
Type I endometrial cancer (EC) is the most common form of EC, displaying less aggressive behavior than type II. The development of type I endometrial cancer is considered a multistep process, with slow progression from normal endometrium to hyperplasia, the premalignant form, and endometrial cancer as a result of an unopposed estrogenic stimulation. The role of mitochondria in type I EC tumor progression and prognosis is currently emerging. This review aims to explore mitochondrial alterations in this cancer and in endometrial hyperplasia focusing on mitochondrial DNA mutations, respiratory complex I deficiency, and the activation of mitochondrial quality control systems. A deeper understanding of altered mitochondrial pathways in type I EC could provide novel opportunities to discover new diagnostic and prognostic markers as well as potential therapeutic targets.
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