MICRORNA-184 AND ITS LNCRNA SPONGE UCA1 ARE INDUCED IN WOUNDED KERATINOCYTES IN A STORE-OPERATED CALCIUM ENTRY-DEPENDENT MANNER

Emerging evidence implicates microRNAs (miRNA) in the regulation of keratinocyte migration. However, the putative roles of microRNA-184 (miR-184) in keratinocyte migration have not been examined. Here, we show that miR-184 expression was elevated following wounding of human keratinocyte monolayers. The induction of miR-184 was dependent on store-operated calcium entry (SOCE) as it was abolished by pharmacologic SOCE blockers. The long non-coding RNA urothelial cancer associated 1 (UCA1), which is thought to acts as a sponge or competing endogenous RNA (ceRNA) against miR-184 was also induced in scratched monolayers. Induction of UCA1 was impaired, but not abolished, by SOCE inhibition. Transfection of keratinocytes with a miR-184 mimic stimulated migration in scratch assays, whereas inhibition of miR-184 dampened the ability of keratinocytes to migrate. Together, our data suggest, for the first time, that SOCE promotes miR-184 induction in wounded monolayers to support keratinocyte migration while also increasing lncRNA UCA1 expression, which may in turn regulate miR-184 activity in keratinocytes.