Long Non-Coding RNAs in Endometrial Carcinoma

International Journal of Molecular Sciences

Maria A. Smolle²  Marc D. Bullock⁴  Hui Ling¹  Martin Pichler³  Johannes Haybaeck² 

[1] Department of Experimental Therapeutics, the University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA;Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, Graz A-8036, Austria;Division of Clinical Oncology, Department of Medicine, Medical University of Graz, Auenbruggerplatz 15, Graz A-8036, Austria;Cancer Sciences, Faculty of Medicine, University of Southampton, Southampton SO171BJ, UK;

关键词: long non-coding RNAs;    endometrial carcinoma;    cancer;   

DOI  :  10.3390/ijms161125962

来源: mdpi

【 摘 要 】

Endometrial carcinoma (EC), the second most common form of gynaecological malignancy, can be divided into two distinct sub-types: Type I tumours arise from hyperplastic endometrium and typically effect women around the time of menopause, whereas type II tumours arise in postmenopausal women from atrophic endometrium. Long non-coding RNAs (lncRNAs) are a novel class of non-protein coding molecules that have recently been implicated in the pathogenesis of many types of cancer including gynaecological tumours. Although they play critical physiological roles in cellular metabolism, their expression and function are deregulated in EC compared with paired normal tissue, indicating that they may also participate in tumour initiation and progression. For instance, the lncRNA MALAT-1 is down-regulated in EC samples compared to normal or hyperplastic endometrium, whereas the lncRNA OVAL is down-regulated in type II disease but up-regulated in type I disease. Other notatble lncRNAs such as HOTAIR, H19 and SRA become up-regulated with increasing EC tumour grade and other features associated with poor prognosis. In the current review, we will examine the growing body of evidence linking deregulated lncRNAs with specific biological functions of tumour cells in EC, we will highlight associations between lncRNAs and the molecular pathways implicated in EC tumourigenesis and we will identify critical knowledge gaps that remain to be addressed.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.