Introduction: MicroRNAs (miRNAs or miRs) control messenger RNA (mRNA) at the post-transcriptional level and have an important role in cancer development. Several studies have demonstrated that miRNAs are capable of regulating other miRNAs, known as a miR-miR interactions. To explore this relatively new idea, we investigated the role of miR-21, a major oncomiR, in initiating miR:miR interactions in head and neck cancer cells. Towards this end, miR-21 was overexpressed and knocked-down. Cells were then sequenced to understand how the expression of miRNAs were altered. This analysis, highlighted that the miR-17-92a cluster is a target of miR-21 regulation. This cluster is highly dysregulated in various cancers, but it is not fully understood how the cluster itself is regulated.
Objective: To investigate the regulatory relationship between miR-21 and the miR-17~92a cluster and the mechanism by which miR-21 regulates the cluster.
Methods and Results: Head and neck cell lines were used as an in vitro cell model to confirm the relationship between miR-21 and the six members of the miR-17~92a cluster. Cells were transfected with miR-21 mimic and antisense and relative fold change of target miRNAs were evaluated using qPCR. Direct regulation of the cluster by miR-21 was then assessed with a luciferase reporter system. To determine if other miRNAs may be regulated by miR-21, a CRISPR knock-out of miR-21 was generated. MicroRNA seq analysis indicated that the miR-21 deletion affected the levels of other miRNAs.
Conclusions: It is proposed that a negative regulatory relationship exists between miR-21 and the miR-17~92a cluster and that miR-21 regulates the cluster by direct binding to the MIR17HG. Furthermore, deletion of miR-21 suggested that other miRNAs may be under the same regulatory control. Our study has provided new information regarding miR:miR interactions in cancer cells and we believe this is an underlying mechanism for controlling miRNA expression.