ArticleBMC complementary medicine and therapies2020
Indirubin inhibits Wnt/β-catenin signal pathway via promoter demethylation of WIF-1.
Article in BMC complementary medicine and therapies, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Dialogue between programmed cell death and psoriasis.Postepy dermatologii i alergologii · 2025Review
- Inhibitors of the Wnt pathway in osteoporosis: A review of mechanisms of action and potential as therapeutic targets.Biomolecules & biomedicine · 2025Review
- Efficacy of indigo naturalis nanofibrous patches in the treatment of chronic plaque psoriasis: a 4-week prospective, randomized, semi-compartmental paired, positive drug-controlled trial.Frontiers in pharmacology · 2025Article
- Evidence and potential mechanism of action of indigo naturalis and its active components in the treatment of psoriasis.Annals of medicine · 2024Review
- A Thia-Analogous IndirubinCells · 2023Article
- Non-additive effect of the DNA methylation inhibitor, 5-Aza-dC, and glass as a culture surface on osteogenic differentiation.Heliyon · 2022Article
- Contribution of the Environment, Epigenetic Mechanisms and Non-Coding RNAs in Psoriasis.Biomedicines · 2022Review
- Anti-tumor necrosis factor drug responses and skin-blood DNA methylation age: Relationships in moderate-to-severe psoriasis.Experimental dermatology · 2021Article
- From natural dye to herbal medicine: a systematic review of chemical constituents, pharmacological effects and clinical applications of indigo naturalis.Chinese medicine · 2020Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPsoriasis is a common inflammatory skin disease. Abnormal proliferation of keratinocytes is one of the psoriatic histopathological features. Indirubin has an essential effect on the proliferation and activation of keratinocytes; however, in psoriasis, the specific mechanism of action of indirubin on keratinocytes is unclear. In the present study, we revealed the effects of indirubin on DNA methyltransferase 1 (DNMT1), wnt inhibitory factor 1 (wif-1), and wnt/β-catenin signal pathway, in the meantime, we explored the effects of indirubin on proliferation, cell cycle and the apoptosis of HaCaT cells.
methodsThe expression of DNMT1, wif-1, Frizzled2, Frizzled5, and β-catenin in HaCaT cells treated with different concentrations of indirubin were detected by Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR). The expression levels of DNMT1 and wif-1 were observed after treated with different concentrations of indirubin by enzyme-linked immunosorbent assay (ELISA). The wif-1 promoter methylation status was detected by DNA methylation-specific PCR (MSP). The transcriptional activities of wif-1 and β-catenin were discovered by a luciferase reporter gene system. Cell viability was determined by Cell Counting Kit-8 (CCK8) method. The cell cycle was detected by flow cytometry. The apoptotic cells were surveyed by the apoptosis kit. The expression of Inolucrin, Loricrin, Filaggrin, Keratin 17, and transcriptional activation of transglutaminase 1(TGase1) were detected by Western blotting.
resultsIndirubin inhibited the expression of DNMT1 and the methylation of the wif-1 promoter. In the wnt signal pathway, indirubin restored the protein expression of wif-1 and inhibited expression of Frizzled2, Frizzled5, and β-catenin. Besides, indirubin inhibited the proliferation of HaCaT cells, induced apoptosis, and arrest cell cycle. We also reported that indirubin could down-regulate the expression of Involucrin, TGase 1, and keratin 17, but the expression of Filaggrin and Loricrin had no significant effect.
conclusionOur research showed that indirubin promoted the demethylation of wif-1 and suppressed the wnt/β-catenin signal pathway, thereby exerted an anti-proliferative effect. This study reveals the anti-proliferation mechanism of indirubin, which may provide an effective option for the treatment of proliferative diseases.
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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.