C-MYC induces idiopathic pulmonary fibrosis via modulation of miR-9-5p-mediated TBPL1

Qin, Hui; Tang, Yan; Yuan, Man; Xue-hui, Zhou; Xu, Tian; Liu, Wenming; Su, Xin

doi:10.1016/j.cellsig.2022.110274

Cited by 16 publications

(10 citation statements)

References 26 publications

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“…Our results showed that the expression of c‐MYC was up‐regulated in pulmonary fibrosis mice and EMT of alveolar epithelial cells. Qin et al, 2022 also found that up‐regulated c‐MYC expression was observed in the lung tissues of IPF mice, which was consistent with our results. In addition, we verified the regulatory effect of c‐MYC on the EMT of alveolar epithelial cells in vitro.…”

Section: Discussionsupporting

confidence: 93%

Emodin inhibiting epithelial‐mesenchymal transition in pulmonary fibrosis through the c‐MYC/miR‐182‐5p/ZEB2 axis

Yang

Jiang

et al. 2022

Phytotherapy Research

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Emodin is a natural anthraquinone compound, which is the main component found in the traditional Chinese herb Polygonum cuspidatum. The anti‐fibrosis effects of Emodin have been reported. This study aimed to explore the specific mechanism of Emodin in the epithelial‐mesenchymal transition (EMT) of pulmonary fibrosis. The pulmonary fibrosis mice models were constructed with bleomycin, the EMT models of alveolar epithelial cells were stimulated by TGF‐β1, and Emodin was used for intervention. c‐MYC and miR‐182‐5p were overexpressed or silenced by cell transfection. Our results demonstrated that Emodin attenuated pulmonary fibrosis induced by bleomycin in mice, and inhibited EMT, meanwhile downregulated c‐MYC, upregulated miR‐182‐5p, and downregulated ZEB2 in vitro and vivo. Next, overexpression of c‐MYC promoted EMT, while silencing c‐MYC and overexpressing miR‐182‐5p inhibited EMT. Then, c‐MYC negatively regulated the expression of miR‐182‐5p with a direct binding relationship. And miR‐182‐5p inhibited ZEB2 expression in a targeted manner. Finally, Emodin inhibited EMT that had been promoted by overexpression of c‐MYC. In conclusion, Emodin could attenuate pulmonary fibrosis and EMT by regulating the c‐MYC/miR‐182‐5p/ZEB2 axis, which might provide evidence for the application of Emodin in the treatment of pulmonary fibrosis.

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Section: Discussionsupporting

confidence: 93%

Emodin inhibiting epithelial‐mesenchymal transition in pulmonary fibrosis through the c‐MYC/miR‐182‐5p/ZEB2 axis

Yang

Jiang

et al. 2022

Phytotherapy Research

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“…The overexpression of c-Myc was identified as a stimulus of proliferation and activation of renal fibroblasts, and targeting c-Myc was shown to be of clinical utility in the treatment of renal fibrosis [ 32 ]. The involvement of c-Myc in fibrosis was also shown in other organs, such as the liver and lung [ 33 , 34 ]. The downregulation of c-Myc observed in our model could explain the absence of obvious signs of fibrosis.…”

Section: Discussionmentioning

confidence: 99%

A Wide-Proteome Analysis to Identify Molecular Pathways Involved in Kidney Response to High-Fat Diet in Mice

Dozio

Maffioli

Vianello

et al. 2022

IJMS

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The etiopathogenesis of obesity-related chronic kidney disease (CKD) is still scarcely understood. To this aim, we assessed the effect of high-fat diet (HF) on molecular pathways leading to organ damage, steatosis, and fibrosis. Six-week-old male C57BL/6N mice were fed HF diet or normal chow for 20 weeks. Kidneys were collected for genomic, proteomic, histological studies, and lipid quantification. The main findings were as follows: (1) HF diet activated specific pathways leading to fibrosis and increased fatty acid metabolism; (2) HF diet promoted a metabolic shift of lipid metabolism from peroxisomes to mitochondria; (3) no signs of lipid accumulation and/or fibrosis were observed, histologically; (4) the early signs of kidney damage seemed to be related to changes in membrane protein expression; (5) the proto-oncogene MYC was one of the upstream transcriptional regulators of changes occurring in protein expression. These results demonstrated the potential usefulness of specific selected molecules as early markers of renal injury in HF, while histomorphological changes become visible later in obesity-related CDK. The integration of these information with data from biological fluids could help the identification of biomarkers useful for the early detection and prevention of tissue damage in clinical practice.

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“…Zuo et al also indicated MMP-7 as the molecules most highly expressed in IPF [32]. At the same time, over-expression of c-Myc, as well as its pivotal role in IPF, have been shown in both in vivo and clinical studies [33,34], which revealed that chronic exposure of mice to SE-PA significantly increased the level of the above-mentioned molecules relevant for pulmonary fibrosis [28,32,33,34,35]. Consequently, presented data as well as disorders in both respiratory function and lung tissue morphology, previously reported by our research team [11], revealed a connection between activation of the Wnt/β-Catenin pathway and development of fibrosis in the course of HP.…”

Section: Discussionmentioning

confidence: 98%

Cathelicidin influence on pathological activation of Wnt pathway in murine model of hypersensitivity pneumonitis

Lemieszek¹,

Golec²,

Zwoliński³

et al. 2022

Ann Agric Environ Med.

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Introduction and Objective. Cathelicidin (CRAMP) is a defence peptide with a wide range of biological responses including antimicrobial, immunomodulatory and wound healing. Furthermore, our previous studies suggested the possibility of using cathelicidin in the prevention and treatment of pulmonary fibrosis in the course of hypersensitivity pneumonitis (HP). The molecular mechanism of CRAMP action, however, was not fully explained. Due to the fact that several studies indicated the Wnt signals pathways as a key player in wound healing and fibrosis, studies focused on this pathway in order to explain the above-mentioned therapeutic potential of cathelicidin in HP development. Materials and method. The study was conducted in a murine model of HP, wherein lung fibrosis is induced in mice strain C57BL/6J by chronic exposure to saline extract of P. agglomerans (SE-PA). Cathelicidin was administered in the an form of aerosol during HP development. Changes in the expression of genes and proteins involved in signals transduction in the Wnt/β-Catenin pathway were examined in lung tissue homogenates by RealTime PCR and Western Blotting, respectively. Results. The study revealed that cathelicidin decreased the elevated level of components of the Wnt/β-Catenin pathway (Ctnnd1/β-Catenin, Wnt1/WNt1, Wnt3a/Wnt3a, Wnt5a/Wnt5a) in the murine model of HP. Furthermore, CRAMP administered together with SE-PA inhibited the transcription function of β-catenin, leading to a decrease in abnormal expression of profibrotic molecules: Cyclin D1, c-Myc, MMP-7. Nevertheless, cathelicidin was not able to completely neutralize the negative changes induced by SE-PA. Conclusions. The study demonstrated the beneficial effect of exogenous cathelicidin on signals transduction in the Wnt/β-Catenin pathway, which may prevent fibrosis development in HP.

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C-MYC induces idiopathic pulmonary fibrosis via modulation of miR-9-5p-mediated TBPL1

Cited by 16 publications

References 26 publications

Emodin inhibiting epithelial‐mesenchymal transition in pulmonary fibrosis through the c‐MYC/miR‐182‐5p/ZEB2 axis

Emodin inhibiting epithelial‐mesenchymal transition in pulmonary fibrosis through the c‐MYC/miR‐182‐5p/ZEB2 axis

A Wide-Proteome Analysis to Identify Molecular Pathways Involved in Kidney Response to High-Fat Diet in Mice

Cathelicidin influence on pathological activation of Wnt pathway in murine model of hypersensitivity pneumonitis

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