circPVT1 promotes silica-induced epithelial-mesenchymal transition by modulating the miR-497-5p/TCF3 axis

Siyun Zhou , Yan Li , Wenqing Sun , Dongyu Ma , Yi Liu , Demin Cheng , Guanru Li , Chunhui Ni

Journal of Biomedical Research ›› 2024, Vol. 38 ›› Issue (2) : 163 -174.

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Journal of Biomedical Research ›› 2024, Vol. 38 ›› Issue (2) :163 -174. DOI: 10.7555/JBR.37.20220249
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circPVT1 promotes silica-induced epithelial-mesenchymal transition by modulating the miR-497-5p/TCF3 axis
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Abstract

Epithelial-mesenchymal transition (EMT) is a vital pathological feature of silica-induced pulmonary fibrosis. However, whether circRNA is involved in the process remains unclear. The present study aimed to investigate the role of circPVT1 in the silica-induced EMT and the underlying mechanisms. We found that an elevated expression of circPVT1 promoted EMT and enhanced the migratory capacity of silica-treated epithelial cells. The isolation of cytoplasmic and nuclear separation assay showed that circPVT1 was predominantly expressed in the cytoplasm. RNA immunoprecipitation assay and RNA pull-down experiment indicated that cytoplasmic-localized circPVT1 was capable of binding to miR-497-5p. Furthermore, we found that miR-497-5p attenuated the silica-induced EMT process by targeting transcription factor 3 (TCF3), an E-cadherin transcriptional repressor, in the silica-treated epithelial cells. Collectively, these results reveal a novel role of the circPVT1/miR-497-5p/TCF3 axis in the silica-induced EMT process in lung epithelial cells. Once validated, this finding may provide a potential theoretical basis for the development of interventions and treatments for pulmonary fibrosis.

Keywords

silicosis / epithelial-mesenchymal transition / circPVT1 / miR-497-5p / TCF3

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Siyun Zhou, Yan Li, Wenqing Sun, Dongyu Ma, Yi Liu, Demin Cheng, Guanru Li, Chunhui Ni. circPVT1 promotes silica-induced epithelial-mesenchymal transition by modulating the miR-497-5p/TCF3 axis. Journal of Biomedical Research, 2024, 38(2): 163-174 DOI:10.7555/JBR.37.20220249

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Fundings

This research was funded by the National Natural Science Foundation of China (Grant No. 82073518).

Acknowledgments

We acknowledge and appreciate our colleagues for their valuable efforts and comments on this paper.

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