Knockdown of lncRNA XIST prevents the epithelial-mesenchymal transition of TGF-β2-induced human lens epithelial cells via miR-124/Slug axis

Jiang, Xue; Zhang, Hong

doi:10.32604/biocell.2022.016167

Cited by 3 publications

(2 citation statements)

References 43 publications

(62 reference statements)

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“…Recently, various cytokine level abnormalities have been found in serum and affected lung tissue in SSc-ILD patients, such as TGF- β 1, TNF- α , and IL-6, and these cytokines are thought to promote fibroblast activation and EMT, which plays a key role in the occurrence of SSc-ILD inflammation and fibrosis [ 28 ]. At present, TGF- β 1 is the most in-depth and important cytokine in the cytokine network involved in SSc-ILD, which regulates the expression of matrix metalloproteinases (MMP) and extracellular matrix (ECM) by activating EMT-related transcription factors to promote epithelial cell apoptosis, migration, and conversion to mesenchymal cells [ 29 , 30 ]. Furthermore, IL-6 and TNF- α are strongly related to the development of lung fibrosis and EMT.…”

Section: Discussionmentioning

confidence: 99%

Scorpion Venom Polypeptide Inhibits Pulmonary Epithelial-Mesenchymal Transition in Systemic Sclerosis-Interstitial Lung Disease Model Mice by Intervening TGF-β1/Smad Signaling Pathway

Zhang

Chen

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Objective. Interstitial lung disease (ILD) is an important complication of systemic sclerosis (SSc). The aim of this study was to investigate the effect and possible mechanism of polypeptide extract of scorpion venom (PESV) on SSc-ILD. Methods. C57/BL6 mice were injected with bleomycin to establish a SSc-ILD model. Different concentrations of PESV solution were administered to SSc-ILD mice, and dexamethasone was used as a positive control. H&E staining and Masson staining were used to observe the pathological changes. The TGF-β1 expression level was detected by immunohistochemistry. The expression of epithelial-mesenchymal transition (EMT)-related proteins was detected by Western blot, and the expression of TGF-β1/Smad pathway-related proteins was also detected. The content of inflammatory cytokines in serum and BALF was determined by ELISA. Results. Pathological analysis showed that PESV could alleviate SSc-ILD-induced pulmonary inflammation and fibrosis. Compared with the model group, the content of inflammatory cytokines IL-6 and TNF-α significantly decreased after PESV treatment. PESV could increase the expression of epithelial marker (E-cadherin) and reduce the expression of interstitial markers (collagen I, vimentin, N-cadherin, and a-SMA). In addition, PESV could reduce the expression level of TGF-β1/Smad pathway-related protein. Conclusion. PESV can attenuate SSc-ILD by regulating EMT, and the effect was linked to the TGF-β1/Smad signaling pathway, which indicated that PESV may serve as a candidate drug for SSc-ILD.

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Section: Discussionmentioning

confidence: 99%

Scorpion Venom Polypeptide Inhibits Pulmonary Epithelial-Mesenchymal Transition in Systemic Sclerosis-Interstitial Lung Disease Model Mice by Intervening TGF-β1/Smad Signaling Pathway

Zhang

Chen

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…Epithelial-mesenchymal transformation (EMT) serves an important function in the metastasis progress of lung cancer cells, and the occurrence of EMT is related to a variety of cytokines, transcription factors, and signal transduction pathways, among which the EMT mediated by TGF-β exerts a pivotal role in metastasis and invasion of NSCLC [7,8]. Polypeptide growth factors secreted by the TGF-β superfamily participated in a variety of pathophysiological processes, including cellular responses, for example, di erentiation, proliferation, and migration [9,10]. TGF-β cell signal transduction is nely regulated at di erent levels, including the regulation of ligands, receptors, SMADs family proteins, and nuclear transcriptional levels [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Keratin 80 Promotes Migration and Invasion of Non-Small Cell Lung Cancer Cells by Regulating the TGF-β/SMAD Pathway

Tong

Chen

Feng

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Upregulation of keratin 80 (KRT80) expression levels and carcinogenic function has been found in several types of tumors. However, its contribution and mechanism in NSCLC remain to be outlined. In this study, bioinformatic investigation from the TCGA dataset revealed that KRT80 was confirmed to be elevated in human NSCLC tissues. The results of qRT-PCR and Western blot assays disclosed that KRT80 was uplifted in NSCLC cells. Data from CCK-8 and colony formation assays exhibited that depletion of KRT80 restrained NSCLC cell proliferation. Findings from Transwell and Western blot assays illustrated that downregulation of KRT80 inhibited NSCLC cell migration, invasion, and EMT. Further mechanism exploration implied that KRT80 may be included within the regulation of EMT of NSCLC cells by affecting the TGF-β/SMAD pathway. Moreover, depletion of KRT80 attenuated xenograft tumor growth and the expressions of KRT80, Ki-67, and TGFBR1. In conclusion, depletion of KRT80 repressed NSCLC cell proliferation, invasion, and EMT, possibly mediated by the TGF-β/SMAD signaling pathway, indicating that KRT80 may be a potentially useful target for NSCLC.

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lncRNA H19 facilitates vascular neointima formation by targeting miR-125a-3p/FLT1 axis

Jiang,

He,

Chen

et al. 2024

ABBS

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The aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) contribute to the development of neointima formation in vascular restenosis. This study aims to explore the function of the long noncoding RNA H19 in neointima formation. A mouse carotid ligation model was established, and human vascular smooth muscle cells (VSMCs) were used as a cell model. lncRNA H19 overexpression promoted VSMC proliferation and migration. Moreover, miR-125a-3p potentially bound to lncRNA H19, and Fms-like tyrosine kinase-1 (FLT1) might be a direct target of miR-125a-3p in VSMCs. Upregulation of miR-125a-3p alleviated lncRNA H19-enhanced VSMC proliferation and migration. Furthermore, rescue experiments showed that enhanced expression of miR-125a-3p attenuated lncRNA H19-induced FLT1 expression in VSMCs. In addition, the overexpression of lncRNA H19 significantly exacerbated neointima formation in a mouse carotid ligation model. In summary, lncRNA H19 stimulates VSMC proliferation and migration by acting as a competing endogenous RNA (ceRNA) of miR-125a-3p. lncRNA H19 may be a therapeutic target for restenosis.

show abstract

Knockdown of lncRNA XIST prevents the epithelial-mesenchymal transition of TGF-β2-induced human lens epithelial cells via miR-124/Slug axis

Cited by 3 publications

References 43 publications

Scorpion Venom Polypeptide Inhibits Pulmonary Epithelial-Mesenchymal Transition in Systemic Sclerosis-Interstitial Lung Disease Model Mice by Intervening TGF-β1/Smad Signaling Pathway

Scorpion Venom Polypeptide Inhibits Pulmonary Epithelial-Mesenchymal Transition in Systemic Sclerosis-Interstitial Lung Disease Model Mice by Intervening TGF-β1/Smad Signaling Pathway

Keratin 80 Promotes Migration and Invasion of Non-Small Cell Lung Cancer Cells by Regulating the TGF-β/SMAD Pathway

lncRNA H19 facilitates vascular neointima formation by targeting miR-125a-3p/FLT1 axis

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