analysis comparing predicted microRNA response elements (MREs) across the CyKILRb and PIK3R2 transcripts identified shared contiguous complementary miRNA binding sequences. Of these miRs, miR-3151-5p, a tumor suppressor and known PIK3R2 regulator, was identified. This miR associated with both RNAs in cells, and treatment of NSCLC cells with a miR-3151-5p mimic reduced PIK3R2 and clonogenicity. Ectopic expression of CyKILRb containing a mutated MRE for miR-3151-5p showed an inability to upregulate PIK3R2 and tumor-promoting phenotypes in contrast to WT CyKILRb. These findings define a novel role for CyKILRb as a competing endogenous RNA for tumor suppressive miRs, which induces the PI3K/AKT axis.
No takes yet. Share an insight, caveat, or question.
Xie et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: