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Key regulator of cellular metabolism, estrogen-related receptor α, a new therapeutic target in endocrine-related gynecological tumor

Authors :
Liu G
Sun P
Dong B
Sehouli J
Source :
Cancer Management and Research, Vol Volume 10, Pp 6887-6895 (2018)
Publication Year :
2018
Publisher :
Dove Medical Press, 2018.

Abstract

GuiFen Liu,1 PengMing Sun,1,2 BinHua Dong,1 Jalid Sehouli3 1Laboratory of Gynaecologic Oncology, Fujian Provincial Maternity and Children’s Hospital, Affiliated Hospital of Fujian Medical University, 350001 Fuzhou, Fujian, People’s Republic of China; 2Department of Gynaecology, Fujian Provincial Maternity and Children’s Hospital, Affiliated Hospital of Fujian Medical University, 350001 Fuzhou, Fujian, People’s Republic of China; 3Department of Gynaecologic Oncology and Gynaecology, Charité/Campus Virchow-Klinikum, European Competence Centre for Ovarian Cancer University of Berlin, Berlin 13353, Germany Abstract: The estrogen-related receptor α (ERRα), is an orphan transcription factor. Recently, many studies have reported its regulatory mechanisms and transcriptional targets after identification. Therefore, it may be eligible to join the rank of other nuclear receptors that control almost all aspects of cell metabolism. Cellular metabolism reprogramming plays a key role in fueling malignant change. The purpose of this review was to demonstrate that the ERRα plays an important role in the association between gynecological endocrine-related tumors and energy metabolism. Furthermore, regulation of ERRα may represent a promising strategy to induce cellular metabolic vulnerability of cancer from different origins. Thus, a comprehensive understanding of current treatment strategies may be achieved. Keywords: orphan receptor, ovarian malignancy, breast malignancy, endometrial malignancy

Details

Language :
English
ISSN :
11791322
Volume :
ume 10
Database :
Directory of Open Access Journals
Journal :
Cancer Management and Research
Publication Type :
Academic Journal
Accession number :
edsdoj.0315d67be334bf9a75d4c2ed33d3a4b
Document Type :
article