LncRNA PFAR contributes to fibrogenesis in lung fibroblasts through competitively binding to miR-15a

Sun, Jian; Su, Wei; Zhao, Xiaojun; Shan, Tianjiao; Jin, Tongzhu; Guo, Yingying; Li, Chao; Li, Ruotong; Zhou, Yuhong; Shan, Hongli; Sun, Xiaobo; Liang, Haihai

doi:10.1042/bsr20190280

Cited by 24 publications

(24 citation statements)

References 27 publications

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“…Numerous studies have reported the emerging role of lncRNAs in the pathogenesis of pulmonary fibrosis ( 19 – 21 ). A previous study found that NEAT1 was increased in human fibrotic liver samples and murine fibrotic livers ( 12 ), while Huang et al ( 13 ) reported that NEAT1 accelerated fibrosis in diabetic nephropathy.…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA‑455‑3p/SMAD3 axis

Liu

Wang

et al. 2021

Mol Med Rep

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Pulmonary fibrosis is an excessive repair response to tissue damage, triggering hyperplasia of fibrotic connective tissues; however, there is no effective treatment in a clinical setting. The purpose of the present study was to investigate the roles of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) and microRNA-455-3p (miR-455-3p) were investigated in pulmonary fibrosis. In this study, the mRNA expression levels of NEAT1, miR-455-3p and SMAD3 in the HPAEpiC alveolar and BEAS-2B bronchial epithelial cell lines were determined using reverse transcription-quantitative PCR, while the markers of epithelial-mesenchymal transformation (EMT) and collagen production were determined using western blot analysis. A wound healing assay was performed to evaluate the migratory ability of the HPAEpiC and BEAS-2B cell lines. The interactions between NEAT1 and miR-455-3p or SMAD3 and miR-455-3p were validated using a luciferase reporter gene assay. The results showed that the mRNA expression levels of NEAT1 and SMAD3 were upregulated in the TGF-β1-treated HPAEpiC and BEAS-2B cell lines, while the mRNA expression level of miR-455-3p was significantly decreased. In addition, silencing NEAT1 effectively alleviated the migratory ability, EMT and collagen generation of the epithelial cells. Following these experiments, NEAT1 was identified as a sponge for miR-455-3p, and SMAD3 was a target gene of miR-455-3p. NEAT1 downregulation or miR-455-3p mimic inhibited the migratory ability, EMT and collagen production of the epithelial cells; however, the effects were reversed by the overexpression of SMAD3. Furthermore, NEAT1 knockdown reduced the expression level of SMAD3 by increasing the expression level of miR-455-3p to further inhibit the migratory ability, EMT and collagen production of epithelial cells.

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Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA‑455‑3p/SMAD3 axis

Liu

Wang

et al. 2021

Mol Med Rep

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“…Accumulating evidence has confirmed that long noncoding RNAs (lncRNAs) are involved in many pathophysiological processes of PF, including cell proliferation, migration, epithelial-mesenchymal transition (EMT), and immunoregulation [7,8]. For example, Song et al found that the abnormal expression of lncRNA and protein-coding gene was associated with the progression of PF through as competing endogenous RNA (ceRNA) [9].…”

Section: Introductionmentioning

confidence: 99%

lncRNA ZFAS1 promotes lung fibroblast-to-myofibroblast transition and ferroptosis via functioning as a ceRNA through miR-150-5p/SLC38A1 axis

Yang

Tai

et al. 2020

Aging

135

108

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Pulmonary fibrosis (PF) is a lethal fibrotic lung disease. The role of lncRNAs in multiple diseases has been confirmed, but the role and mechanism of lncRNA zinc finger antisense 1 (ZFAS1) in the progression of PF need to be elucidated further. Here, we found that lncRNA ZFAS1 was upregulated in bleomycin (BLM)-induced PF rats lung tissues and transforming growth factor-β1 (TGF-β1)-treated HFL1 cells, and positively correlated with the expression of solute carrier family 38 member 1 (SLC38A1), which is an important regulator of lipid peroxidation. Moreover, knockdown of lncRNA ZFAS1 significantly alleviated TGF-β1-induced fibroblast activation, inflammation and lipid peroxidation. In vivo experiments showed that inhibition of lncRNA ZFAS1 abolished BLM-induced lipid peroxidation and PF development. Mechanistically, silencing of lncRNA ZFAS1 attenuated ferroptosis and PF progression by lncRNA ZFAS1 acting as a competing endogenous RNA (ceRNA) and sponging miR-150-5p to downregulate SLC38A1 expression. Collectively, our studies demonstrated the role of the lncRNA ZFAS1/miR-150-5p/SLC38A1 axis in the progression of PF, and may provide a new biomarker for the treatment of PF patients.

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“…Recent studies indicated that lncRNAs acted as a key mediator in various diseases, such as myocardial infarction, pulmonary fibrosis, breast cancer. [21][22][23] Interestingly, lncRNAs were involved in glioma progression. LncRNA PAXIP1-AS1 enhanced migration, invasion, and angiogenesis of human umbilical vein endothelial cells in glioma by recruiting the transcription factor ETS1 to upregulate the expression of KIF14.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway</p>

Zhao¹,

Xue²,

Zhang³

et al. 2020

CMAR

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Purpose: To investigate the specific function of long noncoding RNA FGD5 antisense RNA 1 (lncRNA FGD5-AS1) in glioma. Materials and Methods: The level of FGD5-AS1 was detected in clinical samples and cell lines by qRT-PCR. Small interfering RNA (siRNA) of FGD5-AS1 or scramble siRNA was transfected into U87 cell lines to examine the role of FGD5-AS1 on glioma development. The proliferation of glioma cells was tested by Cell Counting Kit-8 (CCK-8), the migration and invasion of glioma cells were tested by transwell assay without matrigel or with matrigel. Western blot was used to detect the protein expression, and XAV-939 was used to inhibit wnt/β-catenin pathway. The effect of FGD5-AS1 on tumorigenesis of glioma was confirmed by xenograft nude mice model. Results: FGD5-AS1 was significantly increased in glioma tissues and cells. Loss of FGD5-AS1 inhibited the proliferation, migration and invasion of U87 cells. Furthermore, overexpression of FGD5-AS1 increased the mRNA and protein levels of β-catenin and cyclin D1. Blocking of wnt/β-catenin using XAV-939 reversed the promotion role of FGD3-AS1 on glioma cells' migration and invasion. The in vivo tumor growth assay showed that FGD3-AS1 accelerated glioma tumorigenesis with activating wnt/β-catenin pathway. Conclusion: Our research emphasized FGD5-AS1 acting as an oncogene by regulating wnt/ β-catenin signaling pathway, thus providing some novel experimental basis for clinical treatment of glioma.

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LncRNA PFAR contributes to fibrogenesis in lung fibroblasts through competitively binding to miR-15a

Cited by 24 publications

References 27 publications

Long non‑coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA‑455‑3p/SMAD3 axis

Long non‑coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA‑455‑3p/SMAD3 axis

lncRNA ZFAS1 promotes lung fibroblast-to-myofibroblast transition and ferroptosis via functioning as a ceRNA through miR-150-5p/SLC38A1 axis

<p>Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway</p>

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