NF-κB-induced microRNA-31 promotes epidermal hyperplasia by repressing protein phosphatase 6 in psoriasis

Sha, Yan; Xu, Zhenyao; Lou, Fangzhou; Zhang, Lingyun; Fang, Ke; Bai, Jing; Liu, Zhaoyuan; Liu, Jinlin; Wang, Hong; Zhu, Huanhuan; Sun, Yang; Cai, Wei; Gao, Yuanyuan; Su, Bing; Li, Qun; Yang, Xiao; Yu, Jianxiu; Lai, Yuping; Yu, Xue-Zhong; Zheng, Yan; Shen, Nan; Chin, Y. Eugene; Wang, Honglin

doi:10.1038/ncomms8652

Cited by 191 publications

(215 citation statements)

References 45 publications

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“…For instance, miR-31 has been shown to be a direct target of NF-κB in skin keratinocytes leading to hyperproliferation in psoriatic epidermis. 72 In agreement with this, miR-31 was found to be one of the significantly upregulated miRNAs in esophageal hyperplasia induced by zinc deficiency. 73 Furthermore, serine threonine kinase 40 (STK40), a key negative regulator of NF-κB signaling, 74 was shown to be the direct target of miR-31 suggesting a feed forward mechanism by which NF-κB and miR-31 cooperatively promote ESCC proliferation.…”

Section: Non-coding Rnas Regulating/ Regulated By Nf-κb Pathway In Esccsupporting

confidence: 65%

Molecular interplay of pro-inflammatory transcription factors and non-coding RNAs in esophageal squamous cell carcinoma

Sundaram

Bramhachari

2017

Tumour Biol.

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Esophageal squamous cell carcinoma is the sixth most common cancer in the developing world. The aggressive nature of esophageal squamous cell carcinoma, its tendency for relapse, and the poor survival prospects of patients diagnosed at advanced stages, represent a pressing need for the development of new therapies for this disease. Chronic inflammation is known to have a causal link to cancer pre-disposition. Nuclear factor kappa B and signal transducer and activator of transcription 3 are transcription factors which regulate immunity and inflammation and are emerging as key regulators of tumor initiation, progression, and metastasis. Although these pro-inflammatory factors in esophageal squamous cell carcinoma have been well-characterized with reference to protein-coding targets, their functional interactions with noncoding RNAs have only recently been gaining attention. Non-coding RNAs, especially microRNAs and long non-coding RNAs demonstrate potential as biomarkers and alternative therapeutic targets. In this review, we summarize the recent literature and concepts on non-coding RNAs that are regulated by/regulate nuclear factor kappa B and signal transducer and activator of transcription 3 in esophageal cancer progression. We also discuss how these recent discoveries can pave way for future therapeutic options to treat esophageal squamous cell carcinoma.

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Section: Non-coding Rnas Regulating/ Regulated By Nf-κb Pathway In Esccsupporting

confidence: 65%

Molecular interplay of pro-inflammatory transcription factors and non-coding RNAs in esophageal squamous cell carcinoma

Sundaram

Bramhachari

2017

Tumour Biol.

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“…NF-κB is a key determinant in the development of psoriasis through regulation of various proinflammatory cytokines [39,40]. In the present study, we also examined the possible role of NF-κB in anti-psoriatic effect of TC.…”

Section: Discussionmentioning

confidence: 99%

Terminalia Chebulanin Attenuates Psoriatic Skin Lesion via Regulation of Heme Oxygenase-1

Li²,

Dong³

et al. 2016

Cell Physiol Biochem

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Background/Aims: Psoriasis is one of the most common inflammatory skin disorders, affecting 3% of the general population. Terminalia chebulanin (TC) is a polyphenolic compound that possesses antioxidant and anti-inflammatory activities. The current study was designed to investigate the effect of TC on psoriatic lesions. Methods: We examined the protective effect of TC against psoriatic lesions in mice and keratinocyte proliferation in HaCaT cells. Results: We found that TC exhibited potent anti-psoriatic activities, as evidenced by improvement of erythema and scaling scores, decrease of epidermal, ear and skinfold thickening, decrease of tumor necrosis factor α (TNFα), interleukin (IL)-17A, IL-23 and matrix metalloproteinase (MMP)-9 expression, and decrease of TBARS content and increase of GSH content in IMQ-treated mice, and decrease of keratinocyte proliferation, TNFα, IL-17A and IL-23 expression, and ROS level in M5-treated cells. All those effects induced by TC were inhibited by zinc protoporphyrin IX (ZnPP), an inhibitor of heme oxygenase (HO)-1, indicating that HO-1 was responsible the anti-psoriatic effect of TC. Moreover, TC inhibited the upregulation of p65 NF-κB under in vitro psoriatic condition. ZnPP suppressed TC-induced inhibition of p65 NF-κB expression. Overexpression of p65 NF-κB significantly suppressed TC-induced decrease of TNFα, IL-17A and IL-23 expression and keratinocyte proliferation, indicating that HO-1-mediated downregulation of NF-κB was involved in the anti-psoriatic effect of TC. Conclusions: The data demonstrate that TC may serve as a potential therapeutic option for psoriatic patients.

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“…The TNF-α-driven CCL20 release is mediated by keratinocytes and dermal fibroblasts [45]. Upregulation of these proinflammatory cytokines by TNF-α is facilitated through the activation of Nf-κB [46] – a transcription factor that is constitutively activated in psoriatic epidermis [47]. Elevated levels of Nf-κB facilitate keratinocyte hyperproliferation by inhibiting the cell cycle regulator protein, phosphatase 6, via the upregulation of the microRNA miR-31 [47].…”

Section: Resultsmentioning

confidence: 99%

“…Upregulation of these proinflammatory cytokines by TNF-α is facilitated through the activation of Nf-κB [46] – a transcription factor that is constitutively activated in psoriatic epidermis [47]. Elevated levels of Nf-κB facilitate keratinocyte hyperproliferation by inhibiting the cell cycle regulator protein, phosphatase 6, via the upregulation of the microRNA miR-31 [47]. Three TNF-α inhibitors are approved for the treatment of psoriasis: infliximab, adalimumab, and etanercept.…”

Section: Resultsmentioning

confidence: 99%

Psoriasis: Keratinocytes or Immune Cells – Which Is the Trigger?

2018

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Background: Psoriasis is a common, chronic inflammatory skin disorder, which can significantly impact quality of life. Despite major breakthroughs in our understanding of the pathogenesis of psoriasis, the chronological order of the underlying mechanisms leading to the development of psoriatic plaques remains to be completely understood. Summary: Although psoriasis is classically perceived as a T-cell disease, it is now well recognized that T lymphocytes do not function in exclusivity. This theory is supported by evidence from transgenic murine models that develop marked psoriasiform disease. In addition, immune cells and cytokines regulate both early and late events involved in the pathogenesis of psoriasis. Key Messages: Psoriasis is a complex disease – a dynamic interplay between immune cells, keratinocytes, and various other skin-resident cells, such as endothelial and immune cells. The contribution of each cell type is crucial in the initiation and maintenance phases of psoriatic alterations.

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NF-κB-induced microRNA-31 promotes epidermal hyperplasia by repressing protein phosphatase 6 in psoriasis

Cited by 191 publications

References 45 publications

Molecular interplay of pro-inflammatory transcription factors and non-coding RNAs in esophageal squamous cell carcinoma

Molecular interplay of pro-inflammatory transcription factors and non-coding RNAs in esophageal squamous cell carcinoma

Terminalia Chebulanin Attenuates Psoriatic Skin Lesion via Regulation of Heme Oxygenase-1

Psoriasis: Keratinocytes or Immune Cells – Which Is the Trigger?

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