Long Non-Coding RNA-GDA-1 Promotes Keratinocyte Proliferation and Psoriasis Inflammation by Regulating the STAT3/NF-κB Signaling Pathway via Forkhead Box M1
Long Non-Coding RNA-GDA-1 Promotes Keratinocyte Proliferation and Psoriasis Inflammation by Regulating the STAT3/NF-κB Signaling Pathway via Forkhead Box M1
复制标题
长链非编码RNA-GDA-1通过叉头盒M1调控STAT 3/NF-κB信号通路促进角质形成细胞增殖和银屑病炎症
DOI：
10.1007/s10753-023-01800-x
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发表时间：
2023-03
期刊：
影响因子：
5.1
通讯作者：
Xueqing Li;F. Chen;Jiaoying Ju;X-H Yin;Zhenxian Yang;Zhengjun Li;Q. Sun
中科院分区：
文献类型：
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作者：
Xueqing Li;F. Chen;Jiaoying Ju;X-H Yin;Zhenxian Yang;Zhengjun Li;Q. Sun
Psoriasis is a chronic inflammatory skin disease associated with multiple comorbidities and complex pathogenesis. Long non-coding RNAs (lncRNAs) play an important regulatory role in many diseases, including psoriasis. In this study, We aimed to investigate the role and mechanism of lncRNA GDA-1 (GDA) in M5-treated psoriatic keratinocytes. GDA expression was significantly upregulated in psoriatic tissues and M5-treated keratinocytes. By silencing and overexpressing GDA in NHEKs and Ker-CT cells, we showed that GDA regulated proliferation and cell cycle and increased secretion of interleukin‐1β (IL‐1β), IL-6, and chemokine ligands 2 and 20 (CCL2 and CCL20). RNA sequencing after GDA silencing led to the identification of a close regulatory relationship between GDA and Forkhead Box M1 (FOXM1). GDA significantly influenced FOXM1 expression at both mRNA and protein levels and activated STAT3/NF-κB signaling pathways. STAT3 and NF-κB inhibition abrogated GDA effects on keratinocyte proliferation and inflammation. In conclusion, our study is the first to report that Lnc-GDA-1 distinctly regulates FOXM1 expression and mediates proliferation and inflammation of psoriatic keratinocytes through the STAT3/NF-κB signaling pathway, which may be a potent target for psoriasis treatment.
