Department of Dermatology, The First Hospital of Hebei Medical University, Shijiazhuang City, Hebei Province, 050031, China.
Hebei Provincial Innovation Center of Dermatology and Medical Cosmetology Technology, No.89 Donggang Road, Yuhua District, Shijiazhuang City, Hebei Province, China.
Arch Dermatol Res. 2024 Aug 23;316(8):561. doi: 10.1007/s00403-024-03302-8.
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.
环状 RNA（circRNAs）被证明参与了银屑病的进展。circRNAs 可以作为 RNA 结合蛋白（RBP）的海绵。在这里，我们研究了 circAKR1B10 在银屑病中的作用，并探索了与 circAKR1B10 相互作用的潜在蛋白质。通过 qRT-PCR 和 Western blot 分析检测基因和蛋白质的水平。将功能组的角质形成细胞用白细胞介素（IL）-22 处理。分别通过 MTT、5-乙炔基-2'-脱氧尿苷（EdU）和 Transwell 测定进行功能分析。通过生物信息学分析、RNA 下拉测定和 RNA 免疫沉淀（RIP）测定进行 circAKR1B10、真核起始因子 4A-III（EIF4A3）和 Aurora 激酶 A（AURKA）之间的相互作用分析。CircAKR1B10 在银屑病患者和 IL-22 诱导的角质形成细胞中高表达。功能上，circAKR1B10 的敲低消除了 IL-22 诱导的角质形成细胞的增殖、迁移和侵袭。AURKA 的表达在银屑病患者和 IL-22 诱导的角质形成细胞中也更高，并且与 circAKR1B10 的表达呈负相关。此外，AURKA 沉默降低了 IL-22 诱导的角质形成细胞的增殖、迁移和侵袭能力。机制上，circAKR1B10 与 EIF4A3 蛋白相互作用以稳定和调节 AURKA 的表达。CircAKR1B10 通过与 EIF4A3 蛋白相互作用，上调 AURKA 的表达，促进角质形成细胞中 IL-22 诱导的增殖、迁移和侵袭。
