The Role of microRNAs in Epithelial Ovarian Cancer Metastasis

被引:38
|
作者
Nguyen, Vu Hong Loan [1 ]
Yue, Chenyang [1 ]
Du, Kevin Y. [1 ]
Salem, Mohamed [1 ]
O'Brien, Jacob [1 ]
Peng, Chun [1 ,2 ]
机构
[1] York Univ, Dept Biol, Toronto, ON M3J 1P3, Canada
[2] York Univ, Ctr Res Biomol Interact, Toronto, ON M3J 1P3, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
epithelial ovarian cancer; metastasis; microRNAs (miRNAs); FOCAL ADHESION KINASE; TO-MESENCHYMAL TRANSITION; HYPOXIA-INDUCIBLE FACTORS; PREDICTS POOR-PROGNOSIS; INDUCED DOWN-REGULATION; PROMOTES CELL INVASION; UP-REGULATION; TUMOR-SUPPRESSOR; E-CADHERIN; CYCLIN G2;
D O I
10.3390/ijms21197093
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Epithelial ovarian cancer (EOC) is the deadliest gynecological cancer, and the major cause of death is mainly attributed to metastasis. MicroRNAs (miRNAs) are a group of small non-coding RNAs that exert important regulatory functions in many biological processes through their effects on regulating gene expression. In most cases, miRNAs interact with the 3 ' UTRs of target mRNAs to induce their degradation and suppress their translation. Aberrant expression of miRNAs has been detected in EOC tumors and/or the biological fluids of EOC patients. Such dysregulation occurs as the result of alterations in DNA copy numbers, epigenetic regulation, and miRNA biogenesis. Many studies have demonstrated that miRNAs can promote or suppress events related to EOC metastasis, such as cell migration, invasion, epithelial-to-mesenchymal transition, and interaction with the tumor microenvironment. In this review, we provide a brief overview of miRNA biogenesis and highlight some key events and regulations related to EOC metastasis. We summarize current knowledge on how miRNAs are dysregulated, focusing on those that have been reported to regulate metastasis. Furthermore, we discuss the role of miRNAs in promoting and inhibiting EOC metastasis. Finally, we point out some limitations of current findings and suggest future research directions in the field.
引用
收藏
页码:1 / 39
页数:44
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