ArticleCell communication and signaling : CCS2024
The oncogenic kinase TOPK upregulates in psoriatic keratinocytes and contributes to psoriasis progression by regulating neutrophils infiltration.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- TOLLIP Inhibits Psoriasis Progression via Suppressing PKM2-Mediated Glycolysis in Keratinocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Elevated Plasma T-LAK cell-originated protein kinase Owned the Potential for Predicting Favorable Outcomes in Acute Ischemic Stroke Patients.Cellular and molecular neurobiology · 2026Article
- Targeting the TOPK-STAT3 pathway in keratinocytes and mast cells mediates the therapeutic attenuation of Atopic dermatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Activation of unfolded protein response pathways promotes keratinocyte differentiation and ameliorates psoriasis phenotypes.Cell stress & chaperones · 2026Article
- Role of the STAT3 Signaling Pathway in Cell Proliferation and Inflammation in Psoriasis and Approaches for Targeted Therapies: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- Experimental Validation of an Immune Cell Infiltration Signature in Psoriasis: Translating Computational Modeling to In Vivo Efficacy.Journal of clinical laboratory analysis · 2026Article
- Immunomodulatory Effects of a Tick Salivary Serpin on Psoriasis-like Inflammation.Life (Basel, Switzerland) · 2026Article
- The Roles of TOPK in Tumorigenesis and Development: Structure, Mechanisms, Pathways, and Therapeutic Implications.International journal of biological sciences · 2026Review
- Inflammatory immune mechanisms underlying the comorbidity of psoriasis and atherosclerosis: clinical implications.Frontiers in immunology · 2026Review
- From inflammaging to steroid resistance: reframing the pathogenesis of neutrophilic asthma.Frontiers in allergy · 2026Review
- NLRP3-inflammasome Related Genes as Emerging Biomarkers and Therapeutic Targets in Psoriasis.Inflammation · 2025Article
- The Skin-Brain Axis in Psoriasis and Depression: Roles of Inflammation, Hormones, Neuroendocrine Pathways, Neuropeptides, and the Microbiome.Psoriasis (Auckland, N.Z.) · 2025Review
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9 authors.
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Abstract
backgroundT-LAK cell-oriented protein kinase (TOPK) strongly promotes the malignant proliferation of cancer cells and is recognized as a promising biomarker of tumor progression. Psoriasis is a common inflammatory skin disease featured by excessive proliferation of keratinocytes. Although we have previously reported that topically inhibiting TOPK suppressed psoriatic manifestations in psoriasis-like model mice, the exact role of TOPK in psoriatic inflammation and the underlying mechanism remains elusive.
methodsGEO datasets were analyzed to investigate the association of TOPK with psoriasis. Skin immunohistochemical (IHC) staining was performed to clarify the major cells expressing TOPK. TOPK conditional knockout (cko) mice were used to investigate the role of TOPK-specific deletion in IMQ-induced psoriasis-like dermatitis in mice. Flow cytometry was used to analyze the alteration of psoriasis-related immune cells in the lesional skin. Next, the M5-induced psoriasis cell model was used to identify the potential mechanism by RNA-seq, RT-RCR, and western blotting. Finally, the neutrophil-neutralizing antibody was used to confirm the relationship between TOPK and neutrophils in psoriasis-like dermatitis in mice.
resultsWe found that TOPK levels were strongly associated with the progression of psoriasis. TOPK was predominantly increased in the epidermal keratinocytes of psoriatic lesions, and conditional knockout of TOPK in keratinocytes suppressed neutrophils infiltration and attenuated psoriatic inflammation. Neutrophils deletion by neutralizing antibody greatly diminished the suppressive effect of TOPK cko in psoriasis-like dermatitis in mice. In addition, topical application of TOPK inhibitor OTS514 effectively attenuated already-established psoriasis-like dermatitis in mice. Mechanismly, RNA-seq revealed that TOPK regulated the expression of some genes in the IL-17 signaling pathway, such as neutrophils chemokines CXCL1, CXCL2, and CXCL8. TOPK modulated the expression of neutrophils chemokines via activating transcription factors STAT3 and NF-κB p65 in keratinocytes, thereby promoting neutrophils infiltration and psoriasis progression.
conclusionsThis study identified a crucial role of TOPK in psoriasis by regulating neutrophils infiltration, providing new insights into the pathogenesis of psoriasis.
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