Emodin suppresses TGF-β1-induced epithelial-mesenchymal transition in alveolar epithelial cells through Notch signaling pathway

Gao, Rundi; Chen, Ruilin; Cao, Yu; Wang, Yuan; Song, Kyung‐Sik; Zhang, Ya Ping; Junchao, Yang

doi:10.1016/j.taap.2016.12.009

Cited by 36 publications

(24 citation statements)

References 27 publications

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“…In addition, emodin is a main bioactive component of Polygonum cuspidatum that suppressed EMT in alveolar epithelial cells via the Notch signaling pathway. Therefore, it is a promising prospect in treating pulmonary fibrosis . Furthermore, berberine was isolated from Berberis vulgaris and reversed EMT by blocking the Notch/Snail signaling pathway in mice with diabetic nephropathy …”

Section: Small Molecules Against Emtmentioning

confidence: 96%

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Small molecule inhibitors of epithelial‐mesenchymal transition for the treatment of cancer and fibrosis

Feng

Chen

Vaziri

et al. 2019

Medicinal Research Reviews

104

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Tissue fibrosis and cancer both lead to high morbidity and mortality worldwide; thus, effective therapeutic strategies are urgently needed. Because drug resistance has been widely reported in fibrotic tissue and cancer, developing a strategy to discover novel targets for targeted drug intervention is necessary for the effective treatment of fibrosis and cancer. Although many factors lead to fibrosis and cancer, pathophysiological analysis has demonstrated that tissue fibrosis and cancer share a common process of epithelial‐mesenchymal transition (EMT). EMT is associated with many mediators, including transcription factors (Snail, zinc‐finger E‐box‐binding protein and signal transducer and activator of transcription 3), signaling pathways (transforming growth factor‐β1, RAC‐α serine/threonine‐protein kinase, Wnt, nuclear factor‐kappa B, peroxisome proliferator‐activated receptor, Notch, and RAS), RNA‐binding proteins (ESRP1 and ESRP2) and microRNAs. Therefore, drugs targeting EMT may be a promising therapy against both fibrosis and tumors. A large number of compounds that are synthesized or derived from natural products and their derivatives suppress the EMT by targeting these mediators in fibrosis and cancer. By targeting EMT, these compounds exhibited anticancer effects in multiple cancer types, and some of them also showed antifibrotic effects. Therefore, drugs targeting EMT not only have both antifibrotic and anticancer effects but also exert effective therapeutic effects on multiorgan fibrosis and cancer, which provides effective therapy against fibrosis and cancer. Taken together, the results highlighted in this review provide new concepts for discovering new antifibrotic and antitumor drugs.

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Section: Small Molecules Against Emtmentioning

confidence: 96%

“…Therefore, it is a promising prospect in treating pulmonary fibrosis. 96 Furthermore, berberine was isolated from Berberis vulgaris and reversed EMT by blocking the Notch/Snail signaling pathway in mice with diabetic nephropathy. 48…”

Section: Notch Signaling Pathwaymentioning

confidence: 99%

Small molecule inhibitors of epithelial‐mesenchymal transition for the treatment of cancer and fibrosis

Feng

Chen

Vaziri

et al. 2019

Medicinal Research Reviews

104

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“…Silencing Notch1 can intensify the functions of Emodin suppressing TGF-β1-caused EMT in RLE-6TN cells. 16 Considering these previous findings, investigating the factors that might mediate Emodin-induced suppression on Notch1 nuclear translocation and the underlying mechanism is needed.…”

Section: Introductionmentioning

confidence: 99%

“…MI, USA) was firstly dissolved in DMSO (Sigma-Aldrich) and further diluted to 10 µg/ml. 16 The final DMSO concentration was less than 0.1% (v/v). Sivelestat (S7198; Sigma-Aldrich), a neutrophil elastase inhibitor, was used to treat RLE-6TN cells at a density of 100 µg/ ml.…”

Section: Introductionmentioning

confidence: 99%

Emodin inhibiting neutrophil elastase‐induced epithelial‐mesenchymal transition through Notch1 signalling in alveolar epithelial cells

Zhou

Gao

Hong

et al. 2020

J Cellular Molecular Medi

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“…Additionally, activation of Notch pathway has been proven to elevate the microglia-regulated inflammatory response linked to focal cerebral ischemia [37]. Moreover, EMO has been corroborated to restrain TGF-b1-evoked epithelial-mesenchymal transition in alveolar epithelial cells through mediation of Notch pathway [38]. In the actual research, we discovered that EMO enhanced the activations of mTOR and Notch pathways under hypoxia disposition.…”

Section: Discussionmentioning

confidence: 80%

Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells

Cao¹,

Fang

Jia

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Emodin (EMO) possesses extensive pharmacological activities, which has been proven to exert the protective impact in diverse nervous system diseases. Nonetheless, whether EMO emerges a neuro-protective activity in hypoxic-evoked ischemic brain injury is still further probed. The intention of the research is to disclose whether EMO emerges neuro-protective activity in hypoxic-evoked ischemic brain injury. PC-12 received hypoxia administration, and then cell viability, apoptosis and autophagy were estimated. After EMO disposition, the above-involved cellular processes were evaluated again. MiR-25 functions in EMO-affected cells were also estimated. The interrelation between miR-25 and neurofilament light-chain polypeptide gene (NEFL) and the conceivable roles of NEFL in hypoxia-disposed cells were investigated. The latent mechanism was uncovered by mTOR and Notch pathways determination. Hypoxia triumphantly triggered apoptosis and autophagy, but EMO repressed these functions in PC-12 cells. Increased miR-25 was induced by EMO, and inhibited miR-25 abated the impacts of EMO on hypoxia-disposed PC-12 cells. NEFL as a neoteric target gene of miR-25 was predicated, and overexpressed NEFL annulled the functions of EMO in hypoxia-injured cells. EMO activated mTOR and Notch pathways through repressing NEFL. The investigations corroborated that EMO weakened hypoxia-triggered injury via elevating miR-25 by targeting NEFL in PC-12 cells.

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Emodin suppresses TGF-β1-induced epithelial-mesenchymal transition in alveolar epithelial cells through Notch signaling pathway

Cited by 36 publications

References 27 publications

Small molecule inhibitors of epithelial‐mesenchymal transition for the treatment of cancer and fibrosis

Small molecule inhibitors of epithelial‐mesenchymal transition for the treatment of cancer and fibrosis

Emodin inhibiting neutrophil elastase‐induced epithelial‐mesenchymal transition through Notch1 signalling in alveolar epithelial cells

Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells

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