The role and mechanism of lncRNA NEAT1 in the fibrosis of pulmonary epithelial cell

Abstract

Background Pulmonary fibrosis is a serious clinical fatal disease. Epithelial-mesenchymal transition (EMT) and lncRNA NEAT1 have been implied in its development and progression. Objective To study the role of lncRNA NEAT1 in the progression of fibrosis in human pulmonary epithelial cells (BEAS-2B). Specifically, BEAS-2B was transfected with NEAT1 and miR-29c, EMT and cell proliferation were measured and the expression level of relevant genes was determined by Western blot. Result Results showed that NEAT1 promotes fibrosis and proliferation of BEAS-2B cells via the up-regulation of α-SMA, Vimentin, Snail and proliferation-related genes including Cyclin D1 and Cyclin E; miR-29c is a target gene of NEAT1 and through which NEAT1 regulates EMT and expression of proliferation-related genes. Conclusion This study investigated the mechanism of pulmonary fibrosis progression by elucidating the role of NEAT1/ miR-29c in the fibrosis and proliferation of BEAS-2B cells, thus providing a basis for the new therapeutic targets of pulmonary fibrosis.Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Knockdown of long non‑coding RNA NEAT1 relieves inflammation of ulcerative colitis by regulating the miR‑603/FGF9 pathway

“…In addition, NEAT1 contributes to the development of hepatocellular carcinoma by enhancing STAT3 expression and sponging miR-485( 20 ). Furthermore, NEAT1 has been implicated in the disease progression of breast cancer and fibrosis of pulmonary epithelial cells ( 19 , 40 ). Increasing evidence suggest that miR-603 may serve as a tumor suppressor to inhibit tumorigenesis by targeting several signaling enzymes.…”

“…NEAT1 expression is upregulated in liver diseases and different types of cancer ( 18 ). Recently, its aberrant expression has been reported in hepatocellular carcinoma and fibrosis of pulmonary epithelial cells ( 19 , 20 ). However, its role in UC remains unclear.…”

Interaction between long noncoding RNA and microRNA in lung inflammatory diseases

“…In addition, miR‐29b‐2‐5p and miR‐34c‐3p are targets for sponging binding downstream of lnc ATB, upregulating the expression of MEKK2 and NOTCH2, enabling lnc ATB to contribute to the acceleration of the EMT process 78 . Lung epithelial cells express more proliferation and EMT‐related genes when lnc NEAT1 interacts with miR‐29c 79 . lnc RFAL binds to miR‐18a and activates fibroblasts via CTGF to accelerate the process of lung fibrosis, 80 lnc RFAL also suppresses miR‐26a expression, therefore inhibiting miR‐26a's anti‐fibrotic action.…”

“… 78 Lung epithelial cells express more proliferation and EMT‐related genes when lnc NEAT1 interacts with miR‐29c. 79 lnc RFAL binds to miR‐18a and activates fibroblasts via CTGF to accelerate the process of lung fibrosis, 80 lnc RFAL also suppresses miR‐26a expression, therefore inhibiting miR‐26a's anti‐fibrotic action. A mutually inhibitory feedback loop established between miR‐26a and Smad2, leads lnc PFRL to increase fibroblast proliferation and transform into myofibroblast.…”

Interaction between long non-coding RNA and microRNA in lung diseases

“…In addition, miR-29b-2-5p and miR-34c-3p are targets for sponging binding downstream of lnc ATB, upregulating the expression of MEKK2 and NOTCH2, enabling lnc ATB to contribute to the acceleration of the EMT process [114]. Lung epithelial cells express more proliferation and EMT-related genes when lnc NEAT1 interacts with miR-29c [115]. lnc RFAL binds to miR-18a and activates fibroblasts via CTGF to accelerate the process of lung fibrosis [116], lnc RFAL also suppresses miR-26a expression, therefore inhibiting miR-26a's anti-fibrotic action.…”