ArticleCell death & disease2021
Weighted gene coexpression network and experimental analyses identify lncRNA SPRR2C as a regulator of the IL-22-stimulated HaCaT cell phenotype through the miR-330/STAT1/S100A7 axis.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- The long non-coding RNA PVT1 promotes keratinocyte proliferation and inflammation in psoriasis by targeting miR-485-5p.Journal of molecular histology · 2026Article
- Single-Cell RNA Sequencing Revealing Dysregulated Perturbations of Tregs in Psoriasis and Construction of a Treg-Related Diagnostic Model via a 101- Combination Machine Learning Computational FrameworkEndocrine, metabolic & immune disorders drug targets · 2026Article
- A symphony of signals: the intricate role of lncRNAs in dermatological disorders.Clinical and experimental medicine · 2025Review
- Long Non-Coding RNAs in Psoriasis: A Comprehensive Review of Expression Profiles, Mechanistic Insights, Genetic Associations, and Their Clinical Implications.Non-coding RNA · 2025Review
- Long Non-Coding RNAs in Psoriasis and Cutaneous Squamous Cell Carcinoma.Journal of clinical medicine · 2025Review
- BAMBI integrates biostatistical and artificial intelligence methods to improve RNA biomarker discovery.Briefings in bioinformatics · 2025Article
- Biological functions and affected signaling pathways by Long Non-Coding RNAs in the immune system.Non-coding RNA research · 2025Review
- Gene coexpression networks reveal a broad role for lncRNAs in inflammatory bowel disease.JCI insight · 2024Article
- Catechin Protects against Lipopolysaccharide-induced Depressive-like Behaviour in Mice by Regulating Neuronal and Inflammatory Genes.Current gene therapy · 2024Article
- A bibliometrics study on the status quo and hot topics of pathogenesis of psoriasis based on Web of Science.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Article
- Non-Coding RNAs as Potential Targets for Diagnosis and Treatment of Oral Lichen Planus: A Narrative Review.Biomolecules · 2023Review
- Implications of LncRNAs and CircRNAs in psoriasis: a review.RNA biology · 2023Review
- A plasma proteomic approach in patients with heart failure after acute myocardial infarction: insights into the pathogenesis and progression of the disease.Frontiers in cardiovascular medicine · 2023Article
- Non-coding RNAs in immunoregulation and autoimmunity: Technological advances and critical limitations.Journal of autoimmunity · 2023Review
- A Pancancer Analysis of the Oncogenic Role of S100 Calcium Binding Protein A7 (S100A7) in Human Tumors.Biology · 2022Article
- The Role of T Helper 22 Cells in Dermatological Disorders.Frontiers in immunology · 2022Review
- Skin-Expressing lncRNAs in Inflammatory Responses.Frontiers in genetics · 2022Review
- Leucosceptoside A from Devil's Claw Modulates Psoriasis-like Inflammation via Suppression of the PI3K/AKT Signaling Pathway in Keratinocytes.Molecules (Basel, Switzerland) · 2021Article
- Maximizing the Utility of Transcriptomics Data in Inflammatory Skin Diseases.Frontiers in immunology · 2021Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a chronic inflammatory disease of the skin with highly complex pathogenesis. In this study, we identified lncRNA SPRR2C (small proline-rich protein 2C) as a hub gene with a critical effect on the pathogenesis of psoriasis and response to treatment using both weighted gene coexpression network analysis (WGCNA) and differential expression analysis. SPRR2C expression was significantly upregulated in both psoriatic lesion samples and HaCaT cell lines in response to IL-22 treatment. After SPRR2C knockdown, IL-22-induced suppression of HaCaT proliferation, changes in the KRT5/14/1/10 protein levels, and suppression of the IL-1β, IL-6, and TNF-α mRNA levels were dramatically reversed. In the coexpression network with SPRR2C based on GSE114286, miR-330 was significantly negatively correlated with SPRR2C, while STAT1 and S100A7 were positively correlated with SPRR2C. By binding to miR-330, SPRR2C competed with STAT1 and S100A7 to counteract miR-330-mediated suppression of STAT1 and S100A7. MiR-330 overexpression also reversed the IL-22-induced changes in HaCaT cell lines; in response to IL-22 treatment, miR-330 inhibition significantly attenuated the effects of SPRR2C knockdown. STAT1 and S100A7 expression was significantly upregulated in psoriatic lesion samples. The expression of miR-330 had a negative correlation with the expression of SPRR2C, while the expression of SPRR2C had a positive correlation with the expression of STAT1 and S100A7. Thus, SPRR2C modulates the IL-22-stimulated HaCaT cell phenotype through the miR-330/STAT1/S100A7 axis. WGCNA might uncover additional biological pathways that are crucial in the pathogenesis and response to the treatment of psoriasis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.