Psoriasis is a common immune-mediated and genetic skin disease. Forkhead box M1 (FOXM1) is a member of FOX family that has been found to modulate skin disorders. However, its role in psoriasis remains unknown. Thus, we aimed to investigate the effect of FOXM1 on keratinocytes in response to tumor necrosis factor-α (TNF-α). The expression levels of FOXM1 in psoriasis tissues and normal skin tissues were examined using qRT-PCR and western blot. HaCaT cells were stimulated by TNF-α to mimic psoriasis in vitro. MTT assay was performed to assess cell proliferation. The caspase-3 activity and expression levels of bcl-2 and bax were determined to indicate cell apoptosis. The mRNA and secretion levels of IL-6, IL-23 and TGF-β were determined by qRT-PCR and ELISA, respectively. The NF-κB activation was assessed using western blot analysis. Our results demonstrated that FOXM1 was highly upregulated in psoriatic skin tissues and TNF-α-stimulated HaCaT cells. Knockdown of FOXM1 repressed cell proliferation of TNF-α-stimulated HaCaT cells. Knockdown of FOXM1 caused significant increases in caspase-3 activity, bax expression and decrease in bcl-2 expression in TNF-α-stimulated HaCaT cells. Moreover, FOXM1 knockdown also suppressed the TNF-α-induced production of IL-6, IL-23, and TGF-β in HaCaT cells. However, FOXM1 overexpression showed the opposite effect. Furthermore, the TNF-α-induced NF-κB activation was prevented by FOXM1 knockdown. Additionally, inhibition of NF-κB reversed the effects of FOXM1 on HaCaT cells. Taken together, these findings indicated that FOXM1 regulated cell proliferation, apoptosis and inflammation in TNF-α-induced HaCaT cells. The effects of FOXM1 were mediated by NF-κB pathway.

银屑病是一种常见的免疫介导的遗传性皮肤病。Forkhead box M1 (FOXM1) 是 FOX 家族的成员，已被发现可调节皮肤疾病。然而，它在银屑病中的作用仍然未知。因此，我们旨在研究 FOXM1 对角质形成细胞的影响，以响应肿瘤坏死因子-α（TNF-α）。使用 qRT-PCR 和蛋白质印迹检查 FOXM1 在银屑病组织和正常皮肤组织中的表达水平。HaCaT 细胞受 TNF-α 刺激以在体外模拟银屑病. 进行MTT测定以评估细胞增殖。测定 caspase-3 活性和 bcl-2 和 bax 的表达水平以指示细胞凋亡。分别通过qRT-PCR和ELISA测定IL-6、IL-23和TGF-β的mRNA和分泌水平。使用蛋白质印迹分析评估 NF-κB 活化。我们的结果表明 FOXM1 在银屑病皮肤组织和 TNF-α 刺激的 HaCaT 细胞中高度上调。FOXM1 的敲低抑制了 TNF-α 刺激的 HaCaT 细胞的细胞增殖。FOXM1 的敲低导致 TNF-α 刺激的 HaCaT 细胞中 caspase-3 活性、bax 表达和 bcl-2 表达的显着增加。此外，敲低 FOXM1 还抑制了 TNF-α 诱导的 HaCaT 细胞中 IL-6、IL-23 和 TGF-β 的产生。然而，FOXM1 过表达显示出相反的效果。此外，通过 FOXM1 敲低阻止了 TNF-α 诱导的 NF-κB 活化。此外，NF-κB 的抑制逆转了 FOXM1 对 HaCaT 细胞的影响。总之，这些发现表明 FOXM1 在 TNF-α 诱导的 HaCaT 细胞中调节细胞增殖、凋亡和炎症。FOXM1 的作用是由 NF-κB 通路介导的。