Related Experiment Video
Updated: Nov 9, 2025

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
GAS5 regulates viability and apoptosis in TGF-β1-stimulated bronchial epithelial cells by regulating miR-217/HDAC4
Sihui Zhao1, Yunfang Ning1, Na Qin1
1Department of Pediatrics, Heping Hospital Affiliated to Changzhi Medical College, No. 110, Yanan Sourth Road, Changzhi, 046000, Shanxi Province, China.
Background:
Asthma is a serious respiratory disease that affects the physical and mental health of children. Airway epithelial apoptosis concomitantly mediated by transforming growth factor-β1 (TGF-β1) is a crucial component of asthma pathogenesis. LncRNA growth Arrest Specific 5 (GAS5), microRNA-217 (miR-217) and Histone deacetylase 4 (HDAC4) shown a close relationship with TGF-β1-induced injury of airway epithelial. However, the mechanism underlying TGF-β1-induced injury of airway epithelial in asthma still needs to be investigated.
Objective:
We aimed to investigate the effect and underlying mechanism of GAS5/miR-217/HDAC4 axis in TGF-β1-stimulated bronchial epithelial cells.
Methods:
The levels of were detected by quantitative real-time polymerase chain reaction (RT-qPCR). All protein levels were determined by western blot. Cell viability and apoptosis rate were assessed by Methyl thiazolyl tetrazolium (MTT) and Flow cytometry, respectively. The targeting relationship between miR-217 and GAS5 or HDAC4 was examined with dual-luciferase reporter assay.
Results:
TGF-β1, GAS5, HDAC4 were up-regulated, while miR-217 was down-regulated in bronchial mucosal tissues of asthmatic children and TGF-β1-treated BEAS-2B cells. TGF-β1 could reduce cell viability and induce apoptosis, while these effects could be reversed by downregulation of GAS5 or HDAC4. Mechanically, GAS5 acted as a sponge for miR-217 to regulate the expression of HDAC4. Furthermore, overexpression of HDAC4 rescued the effects of GAS5 knockdown on viability and apoptosis of TGF-β1-induced BEAS-2B cells. GAS5 knockdown induced cell viability and hampered cell apoptosis in TGF-β1-stimulated BEAS-2B cells by regulating the miR-217/HDAC4 axis.
Conclusions:
The lncRNA GAS5/miR-217/HDAC4 axis played an important role in regulating TGF-β1-induced bronchial epithelial cells injury, thus contributing to asthma.
More Related Videos
06:02Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition
Published on: June 10, 2016
10:49Efficient Transcriptionally Controlled Plasmid Expression System for Investigation of the Stability of mRNA Transcripts in Primary Alveolar Epithelial Cells
Published on: March 6, 2020
Related Concept Videos
TGF - β Signaling Pathway
Regulation of Angiogenesis and Blood Supply
Apoptosis
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
Hedgehog Signaling Pathway
Negative Regulator Molecules