Bai Wanting, Wang Kunqin, Wu Shaobo, Zhou Xiaolin, Liu Luyu, Liu Meng, Chen Caifeng
Department of Dermatology, Fujian Provincial Hospital, Clinical Medical College of Fujian Medical University, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian, China.
Department of Dermatology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, Shaanxi, China.
Sci Rep. 2025 Aug 7;15(1):28929. doi: 10.1038/s41598-025-13992-3.
Anoikis is a programmed cell death that occurs when cells detach from the extracellular matrix (ECM). Its role in psoriasis remains unclear. This study aims to explore the relationship between psoriasis and apoptosis, focusing on anoikis-related mechanisms. Differentially expressed genes (DEGs) in psoriasis were identified using the GEO database and overlapped with anoikis-related genes from GeneCards to find differentially expressed anoikis-related genes (DE-ARGs). A PPI network was constructed, revealing eight hub DE-ARGs. These were then analyzed using GO, KEGG and ssGSEA. Immune infiltration cells and molecules were examined, and single-cell data analysis, immunohistochemistry, qRT-PCR, Western blotting, gene mapping, and drug prediction were performed. Eighteen DE-ARGs were identified, with STAT3 and BIRC5 as key DEGs. Enrichment analysis showed DE-ARGs were related to the regulation of anoikis and positive regulation of epithelial cell proliferation. Notable differences in dendritic and mast cells were observed between psoriasis lesions and no-lesion samples. Elevated expression of BIRC5 and STAT3 in psoriasis lesions was confirmed through qRT-PCR, western blotting and immunohistochemistry. This study establishes a relationship between anoikis and psoriasis, where STAT3 and BIRC5 play important roles. STAT3 and BIRC5 may serve as potential targets for the prevention and treatment of psoriasis.
失巢凋亡是一种程序性细胞死亡，发生于细胞与细胞外基质（ECM）脱离时。其在银屑病中的作用尚不清楚。本研究旨在探讨银屑病与细胞凋亡之间的关系，重点关注与失巢凋亡相关的机制。利用GEO数据库鉴定银屑病中差异表达基因（DEGs），并与来自GeneCards的失巢凋亡相关基因进行重叠，以找到差异表达的失巢凋亡相关基因（DE-ARGs）。构建了蛋白质-蛋白质相互作用（PPI）网络，揭示了8个枢纽DE-ARGs。随后使用基因本体论（GO）、京都基因与基因组百科全书（KEGG）和单样本基因集富集分析（ssGSEA）对这些基因进行分析。检测了免疫浸润细胞和分子，并进行了单细胞数据分析、免疫组织化学、定量逆转录聚合酶链反应（qRT-PCR）、蛋白质免疫印迹法（Western blotting）、基因定位和药物预测。鉴定出18个DE-ARGs，其中信号转导和转录激活因子3（STAT3）和凋亡抑制蛋白5（BIRC5）为关键DEGs。富集分析表明，DE-ARGs与失巢凋亡的调控及上皮细胞增殖的正调控有关。在银屑病皮损和非皮损样本之间观察到树突状细胞和肥大细胞存在显著差异。通过qRT-PCR、蛋白质免疫印迹法和免疫组织化学证实了银屑病皮损中BIRC5和STAT3的表达升高。本研究建立了失巢凋亡与银屑病之间的关系，其中STAT3和BIRC5发挥重要作用。STAT3和BIRC5可能作为银屑病预防和治疗的潜在靶点。
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