Role of circular RNAs in retinoblastoma

Li, Fēi; Yin, Yi-Ke; Zhang, Jitao; Gong, Hai-Pai; Hao, Xiaodan

doi:10.1007/s10142-022-00942-9

Cited by 6 publications

(1 citation statement)

References 115 publications

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“…In prostate cancer, circMKLN1 was significantly associated with patient prognosis and has good potential for biomarker application (Hansen et al 2022 ). In retinoblastoma, circMKLN1 could play a tumor suppressive role, and the mechanism may be through sponge adsorption of miR-425-5p, which in turn promotes PDCD4 and inhibits proliferation, migration and invasion of tumor cells (Li et al 2022 ; Xu et al 2021 ). In this study, we demonstrated that inhibition of circMKLN1 significantly reduced pulmonary fibrosis and EMT in vivo and in vitro.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA MKLN1 promotes epithelial-mesenchymal transition in pulmonary fibrosis by regulating the miR-26a/b-5p/CDK8 axis in human alveolar epithelial cells and mice models

Zhu,

Meng,

Zhu

et al. 2024

Arch Toxicol

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Pulmonary fibrosis involves destruction of the lung parenchyma and extracellular matrix deposition. Effective treatments for pulmonary fibrosis are lacking and its pathogenesis is still unclear. Studies have found that epithelial-mesenchymal transition (EMT) of alveolar epithelial cells (AECs) plays an important role in progression of pulmonary fibrosis. Thus, an in-depth exploration of its mechanism might identify new therapeutic targets. In this study, we revealed that a novel circular RNA, MKLN1 (circMKLN1), was significantly elevated in two pulmonary fibrosis models (intraperitoneally with PQ, 50 mg/kg for 7 days, and intratracheally with BLM, 5 mg/kg for 28 days). Additionally, circMKLN1 was positively correlated with the severity of pulmonary fibrosis. Inhibition of circMKLN1 expression significantly reduced collagen deposition and inhibited EMT in AECs. EMT was aggravated after circMKLN1 overexpression in AECs. MiR-26a-5p/miR-26b-5p (miR-26a/b), the targets of circMKLN1, were confirmed by luciferase reporter assays. CircMKLN1 inhibition elevated miR-26a/b expression. Significantly decreased expression of CDK8 (one of the miR-26a/b targets) was observed after inhibition of circMKLN1. EMT was exacerbated again, and CDK8 expression was significantly increased after circMKLN1 inhibition and cotransfection of miR-26a/b inhibitors in AECs. Our research indicated that circMKLN1 promoted CDK8 expression through sponge adsorption of miR-26a/b, which regulates EMT and pulmonary fibrosis. This study provides a theoretical basis for finding new targets or biomarkers in pulmonary fibrosis.

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Section: Discussionmentioning

confidence: 99%