ArticleCell cycle (Georgetown, Tex.)2020
miR-203 promotes HaCaT cell overproliferation through targeting LXR-α and PPAR-γ.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Gut microbiota-induced perturbation in bile acids alter keratinocyte lipid metabolism via FXR-NQO1 signaling in psoriasis.Nature communications · 2026Article
- Umbilical Cord Mesenchymal Stem Cells as a Meritorious Option to Treat Psoriasis.Current stem cell research & therapy · 2026Review
- MicroRNAs in immune-related diseases: mechanism, functions and therapeutic perspectives.Frontiers in immunology · 2026Review
- Psoriasis Treatments: Emerging Roles and Future Prospects of MicroRNAs.Non-coding RNA · 2025Review
- miRNAs and exosomes in psoriasis: coordinating cytoskeleton dynamics and extracellular matrix remodeling.Frontiers in cell and developmental biology · 2025Review
- The Role of Epigenetic Factors in the Pathogenesis of Psoriasis.International journal of molecular sciences · 2024Review
- Expression profile of mRNAs and miRNAs related to mitogen-activated kinases in HaCaT cell culture treated with lipopolysaccharide a and adalimumab.Cell cycle (Georgetown, Tex.) · 2024Article
- Multi-Omics Approach to Improved Diagnosis and Treatment of Atopic Dermatitis and Psoriasis.International journal of molecular sciences · 2024Review
- Identification and functional validation of SRC and RAPGEF1 as new direct targets of miR-203, involved in regulation of epidermal homeostasis.Scientific reports · 2023Article
- Genetic and Epigenetic Mechanisms of Psoriasis.Genes · 2023Review
- Expression Signature of Immune-Related MicroRNAs in Autoimmune Skin Disease: Psoriasis and Vitiligo Insights.Molecular diagnosis & therapy · 2023Article
- Emerging roles of non-coding RNAs in psoriasis pathogenesis.Functional & integrative genomics · 2023Review
- Peroxisome proliferator-activator receptor γ and psoriasis, molecular and cellular biochemistry.Molecular and cellular biochemistry · 2022Review
- The lncRNA PRINS-miRNA-mRNA Axis Gene Expression Profile as a Circulating Biomarker Panel in Psoriasis.Molecular diagnosis & therapy · 2022Article
- Identification of potential key molecules and signaling pathways for psoriasis based on weighted gene co-expression network analysis.World journal of clinical cases · 2022Article
- Circulating microRNA203 and its target genes' role in psoriasis pathogenesis.Frontiers in medicine · 2022Article
- Maximizing the Utility of Transcriptomics Data in Inflammatory Skin Diseases.Frontiers in immunology · 2021Review
- miRNAs Flowing Up and Down: The Concerto of Psoriasis.Frontiers in medicine · 2021Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is an immune-mediated chronic inflammatory skin disease. Keratinocyte hyperproliferation has been regarded as a significant event in psoriasis pathogenesis. Considering the vital role of miRNA-mediated mRNA repression in psoriasis pathogenesis, in the present study, we attempted to investigate the mechanism of keratinocyte overproliferation from the point of miRNA-mRNA regulation. Both online microarray expression profiles and experimental results indicated that the expression of LXR-α and PPAR-γ was downregulated in psoriasis lesion skin. LXR-α or PPAR-γ overexpression alone was sufficient to inhibit keratinocyte proliferation, decrease KRT5 and KRT14 protein levels and increase KRT1 and KRT10 protein levels. miR-203 negatively regulated LXR-α and PPAR-γ expression through direct targeting. miR-203 inhibition exerted the opposite effects to LXR-α or PPAR-γ overexpression on HaCaT cells. More importantly, LXR-α or PPAR-γ overexpression could markedly remarkably attenuate the effects of miR-203 overexpression in keratinocytes, indicating that miR-203 promotes keratinocyte proliferation by targeting LXR-α and PPAR-γ. In conclusion, the miR-203-LXR-α/PPAR-γ axis modulates the proliferation of keratinocytes and might be a novel target for psoriasis treatment, which needs further in vivo investigation.
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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.