Exploring the Potential of MicroRNA Let-7c as a Therapeutic for Prostate Cancer
Prostate cancer (PCa) is one of the leading causes of mortality worldwide and often presents with aberrant microRNA (miRNA) expression. Identifying and understanding the unique expression profiles could aid in the detection and treatment of this disease. This review aims to identify miRNAs as potent...
Saved in:
Published in | Molecular therapy. Nucleic acids Vol. 18; pp. 927 - 937 |
---|---|
Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
06.12.2019
Elsevier Limited American Society of Gene & Cell Therapy Elsevier |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Prostate cancer (PCa) is one of the leading causes of mortality worldwide and often presents with aberrant microRNA (miRNA) expression. Identifying and understanding the unique expression profiles could aid in the detection and treatment of this disease. This review aims to identify miRNAs as potential therapeutic targets for PCa. Three bio-informatic searches were conducted to identify miRNAs that are reportedly implicated in the pathogenesis of PCa. Only hsa-Lethal-7 (let-7c), recognized for its role in PCa pathogenesis, was common to all three databases. Three further database searches were conducted to identify known targets of hsa-let-7c. Four targets were identified, HMGA2, c-Myc (MYC), TRAIL, and CASP3. An extensive review of the literature was undertaken to assess the role of hsa-let-7c in the progression of other malignancies and to evaluate its potential as a therapeutic target for PCa. The heterogeneous nature of cancer makes it logical to develop mechanisms by which the treatment of malignancies is tailored to an individual, harnessing specific knowledge of the underlying biology of the disease. Resetting cellular miRNA levels is an exciting prospect that will allow this ambition to be realized.
[Display omitted] |
---|---|
Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 2162-2531 2162-2531 |
DOI: | 10.1016/j.omtn.2019.09.031 |