Abstract
Majority of the human genome is transcribed to RNAs that do not encode proteins. These non-coding RNAs (ncRNAs) play crucial roles in regulating the initiation and progression of various cancers. Given the importance of the ncRNAs, the roles of ncRNAs in cancers have been reviewed elsewhere. Thus, in this review, we mainly focus on the recent studies of the function, regulatory mechanism and therapeutic potential of the ncRNAs including microRNA (miRNA), long ncRNA (lncRNA), circular RNA (circRNA) and PIWI interacting RNA (piRNA), in different type of cancers.
Highlights
Approx. 75% of the human genome is transcribed into RNA, while only 3% is transcribed into protein-coding mRNAs [1]
In this review, we mainly focus on the recent studies of the function, regulatory mechanism and therapeutic potential of the non-coding RNA (ncRNA) including microRNA, long ncRNA, circular RNA and PIWI interacting RNA, in different type of cancers
MicroRNA, long ncRNA, circular RNA and PIWI interacting RNA are the four major ncRNA types with distinct functions in cancers. miRNAs are a kind of small RNA with approx. 22 nucleotides in length. miRNAs bind to the complementary sequence in targeted mRNA and cause RNA-induced silencing complex (RISC) to degrade targeted mRNA (Figure 1) [2]. piRNA was first identified in Drosophila with 24–30 nt in length
Summary
Approx. 75% of the human genome is transcribed into RNA, while only 3% is transcribed into protein-coding mRNAs [1]. Let-7 miRNAs target and down-regulate many oncogenic genes including E2F1, ARID3B, K-RAS and c-Myc, resulting in suppression of tumor progression [25]. All the nine miRNAs have been identified as tumor suppressors and suppressed by circHIPK3 [54] These studies demonstrate that the expression of circRNAs is dynamically regulated in different cancers, and regulates cancer progression through distinct mechanisms. Li et al took a computational approach to design and identify small molecules on the base of the predicted miRNA hairpin precursor structures They found that a benzimidazole analog selectively inhibited the processing of pri-miR-96 into oncogenic miR-96 and elevated miR-96 target gene expression and promoted cancer cell apoptosis [64]. Another dimeric benzimidazole and bisbenzimide analog, targaprimir (TGP)-515, is
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