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. 2024 Aug 23;316(8):561.
doi: 10.1007/s00403-024-03302-8.

CircAKR1B10 interacts with EIF4A3 to stabilize AURKA and promotes IL-22-induced proliferation, migration and invasion in keratinocytes

Liping Shi  1   2 , Xiaoqing Du  3 , Bin Wang  1   2 , Guoqiang Zhang  4   5
Affiliations

CircAKR1B10 interacts with EIF4A3 to stabilize AURKA and promotes IL-22-induced proliferation, migration and invasion in keratinocytes

Liping Shi et al. Arch Dermatol Res. .

Abstract

Circular RNAs (circRNAs) are demonstrated to be involved in psoriasis progression. CircRNAs can act as RNA-binding protein (RBP) sponges. Here, we investigated the action of circAKR1B10 in psoriasis, and explored the potential proteins interacted with circAKR1B10. Levels of genes and proteins were assayed by qRT-PCR and western blotting analyses. Keratinocytes in functional groups were treated with interleukin (IL)-22. Functional analysis were conducted using MTT, 5-ethynyl-2'-deoxyuridine (EdU), and transwell assays, respectively. Interaction analysis among circAKR1B10, Eukaryotic initiation factor 4 A-III (EIF4A3) and Aurora Kinase A (AURKA) was conducted using bioinformatics analysis, RNA pull-down assay, and RNA immunoprecipitation (RIP) assay. CircAKR1B10 was highly expressed in psoriasis patients and IL-22-induced keratinocytes. Functionally, knockdown of circAKR1B10 abolished IL-22-induced proliferation, migration and invasion in keratinocytes. AURKA expression was also higher in psoriasis patients and IL-22-induced keratinocytes, and was negatively correlated with circAKR1B10 expression. Moreover, AURKA silencing reduced the proliferative, migratory and invasive abilities of IL-22-induced keratinocytes. Mechanistically, circAKR1B10 interacted with EIF4A3 protein to stabilize and regulate AURKA expression. CircAKR1B10 contributes to IL-22-induced proliferation, migration and invasion in keratinocytes via up-regulating AURKA expression through interacting with EIF4A3 protein.

Keywords: AURKA; EIF4A3; IL-22; Keratinocytes; Psoriasis; circAKR1B10.

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