Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Department of Pulmonary and Critical Care Medicine, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
DNA Cell Biol. 2021 Jan;40(1):18-25. doi: 10.1089/dna.2020.6030. Epub 2020 Dec 11.
Pulmonary fibrosis (PF) is a progressive and lethal disease with poor prognosis. plays an important role in the progression of cancer. However, the role of in PF has not yet been reported. In this study, we explored the potential role of in PF and its potential molecular mechanisms. Increased expression of was first observed in lung tissues of PF patients. We found that downregulation of inhibited the transforming growth factor-β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) in A549 cells. Mechanically, TGF-β1 upregulated β-catenin and the phosphorylation of glycogen synthase kinase-3β, which was blocked by silencing . Furthermore, lithium chloride (activator of the Wnt/β-catenin signaling pathway) effectively rescued knockdown-mediated inhibition of EMT in PF. In conclusion, these findings demonstrate that downregulation of alleviated PF through inhibiting EMT. is a promising potential target for further understanding the mechanism and developing a strategy for the treatment of PF and other EMT-associated diseases.
肺纤维化（PF）是一种进行性和致命性疾病，预后不良。在癌症的进展中起着重要作用。然而，在 PF 中 的作用尚未被报道。在这项研究中，我们探讨了 在 PF 中的潜在作用及其潜在的分子机制。首先观察到 PF 患者肺组织中 的表达增加。我们发现下调 抑制了 A549 细胞中转化生长因子-β1（TGF-β1）诱导的上皮-间充质转化（EMT）。在机制上，TGF-β1 上调了β-连环蛋白和糖原合成酶激酶-3β的磷酸化，这被 沉默所阻断。此外，氯化锂（Wnt/β-连环蛋白信号通路的激活剂）有效地挽救了 敲低介导的 PF 中 EMT 的抑制。总之，这些发现表明下调 通过抑制 EMT 缓解 PF。 是进一步了解机制和开发治疗 PF 及其他 EMT 相关疾病策略的有希望的潜在靶点。
