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Multiple Roles of MicroRNA-100 in Human Cancer and its Therapeutic Potential

Chen LiDepartment of Medical Oncology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, ChinaYanping GaoDepartment of Medical Oncology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, ChinaKai ZhangDepartment of Medical Oncology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, ChinaJing ChenDepartment of Medical Oncology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, ChinaSiqi HanDepartment of Medical Oncology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, ChinaBing FengDepartment of Medical Oncology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, ChinaRui WangDepartment of Medical Oncology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, ChinaLongbang ChenDepartment of Medical Oncology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China

2015en

ABI

Annotatsiya

MicroRNAs (miRNAs) are a recently discovered class of endogenous, small (about 22 nucleotides) non-coding RNAs, which play important roles in cancer development and progression. Emerging evidence shows that microRNAs exert their regulatory effects by directly binding to the 3'- untranslated regions (UTRs) of their target genes. MicroRNA-100 (miR-100) is aberrantly expressed and functions in many human cancers by regulating multiple cell processes, such as cell cycle, proliferation, differentiation, migration, invasion and apoptosis, via post-transcriptionally regulating various target genes. A better understanding of the molecular mechanisms involved in miR-100-mediated tumor progression will provide an opportunity for exploring novel miR-100-based targeted therapies for human cancers. This review aims to summarize the recently published literature on the roles of miR-100 in regulating tumorigenesis, and explore its potential clinical applications for cancer diagnosis, prognosis and clinical treatment.

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DOI: 10.1159/000438572

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