Demonstrating the specificity of these effects, co-transfection with a miR-18a mimic actually diminished downregulation of the wild-type reporters, possibly by competing for limiting miRNA pathway components and thereby relieving the transcript from repression. These data document that miR-26a directly represses expression of cyclin D2 and cyclin E2, providing one mechanism through which this miRNA arrests cell-cycle progression.
More recently, the investigators[77] focused on miR-26a whose expression is most significantly perturbed in MYC-induced liver cancer model. Mir-26a targets expression of cyclins D2 and E2; and ectopic expression of miR-26a induced G1 arrest in HepG2 hepatcocellular carcinoma cell line.