Abstract
A subset of oxidative stress-induced miRNAs is involved in AKT signaling in uterine leiomyoma. Overexpression of miR-181a and miR-182 resulted in cellular senescence in leiomyoma through repression of AKT3 and CCND2, respectively. Silencing of AKT3 and CCND2 drives leiomyoma cell into senescence and cycle arrest. Application of our newly developed 3D leiomyoma spheroids can provide a quick and reliable ex vivo model for cytopathologic and functional analysis. BH3 mimetics can effectively reduce the viability of miRNA-mediated senescent cells in leiomyoma.
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