Tectorigenin regulates migration, invasion, and apoptosis in dexamethasone‐induced human airway epithelial cells through up‐regulating miR‐222‐3p

Glucocorticoids (GCs) can effectively control airway inflammation, but can also cause airway epithelial injury. Tectorigenin, a type of isoflavone isolated from various medicinal plants, has hypolipidemic activity, hepatoprotective, and antioxidant effects. We aimed to investigate whether Tectorigen...

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Published inDrug development research Vol. 82; no. 7; pp. 959 - 968
Main Authors Qian, Xiong, Xiao, Qi, Li, Zongqi
Format Journal Article
LanguageEnglish
Published Hoboken, USA John Wiley & Sons, Inc 01.11.2021
Wiley Subscription Services, Inc
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ISSN0272-4391
1098-2299
1098-2299
DOI10.1002/ddr.21795

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Abstract Glucocorticoids (GCs) can effectively control airway inflammation, but can also cause airway epithelial injury. Tectorigenin, a type of isoflavone isolated from various medicinal plants, has hypolipidemic activity, hepatoprotective, and antioxidant effects. We aimed to investigate whether Tectorigenin can repair GCs‐induced airway epithelial injury. Airway epithelial cell line (9HTE cells) were treated with dexamethasone (Dex), Tectorigenin, or further transfected, then cell viability, migration, and invasion were examined by Cell Counting Kit (CCK‐8), wound healing, and Transwell assays. The expressions of potential miRNAs related to the effect of Tectorigenin were detected by quantitative polymerase chain reaction (qPCR). Expressions of poptosis‐related proteins Bcl‐2‐associated protein‐X (Bax), B‐cell lymphoma‐2 (Bcl‐2), Cleaved Caspase‐3, and related to Mitorgen‐activated protein kinase (MAPK) signaling pathway serine/threonine kinase (Raf1), extracellular signal‐regulated kinase kinase 1/2 (MEK1/2), and extracellular signal‐regulated kinase 1/2 (ERK1/2) were detected by Western blot. Dex inhibited the cell viability, migration and invasion by promoting Bax and Cleaved Caspase‐3 expressions (p <.001) and by inhibiting the expressions of Bcl‐2 and miR‐222‐3p (p <.001). Then, 10 μmol/L Tectorigenin itself did not affect cell viability but could inhibit the effect of Dex on cell viability, migration, and invasion. Tectorigenin up‐regulated the expressions of miR‐222‐3p, Bcl‐2, p‐Raf1, p‐MEK1/2, and p‐ERK1/2 (p <.01), but down‐regulated the expressions of Bax and Cleaved Caspase‐3 (p <.05) in Dex‐induced cells. MiR‐222‐3p inhibitor reversed the antagonistic effect of Tectorigenin on Dex. The study demonstrates that Tectorigenin inhibits apoptosis of Dex‐induced 9HTE cells by up‐regulating the expression of miR‐222‐3p, which involves with the MAPK pathway.
AbstractList Glucocorticoids (GCs) can effectively control airway inflammation, but can also cause airway epithelial injury. Tectorigenin, a type of isoflavone isolated from various medicinal plants, has hypolipidemic activity, hepatoprotective, and antioxidant effects. We aimed to investigate whether Tectorigenin can repair GCs‐induced airway epithelial injury. Airway epithelial cell line (9HTE cells) were treated with dexamethasone (Dex), Tectorigenin, or further transfected, then cell viability, migration, and invasion were examined by Cell Counting Kit (CCK‐8), wound healing, and Transwell assays. The expressions of potential miRNAs related to the effect of Tectorigenin were detected by quantitative polymerase chain reaction (qPCR). Expressions of poptosis‐related proteins Bcl‐2‐associated protein‐X (Bax), B‐cell lymphoma‐2 (Bcl‐2), Cleaved Caspase‐3, and related to Mitorgen‐activated protein kinase (MAPK) signaling pathway serine/threonine kinase (Raf1), extracellular signal‐regulated kinase kinase 1/2 (MEK1/2), and extracellular signal‐regulated kinase 1/2 (ERK1/2) were detected by Western blot. Dex inhibited the cell viability, migration and invasion by promoting Bax and Cleaved Caspase‐3 expressions ( p <.001) and by inhibiting the expressions of Bcl‐2 and miR‐222‐3p ( p <.001). Then, 10 μmol/L Tectorigenin itself did not affect cell viability but could inhibit the effect of Dex on cell viability, migration, and invasion. Tectorigenin up‐regulated the expressions of miR‐222‐3p, Bcl‐2, p‐Raf1, p‐MEK1/2, and p‐ERK1/2 ( p <.01), but down‐regulated the expressions of Bax and Cleaved Caspase‐3 ( p <.05) in Dex‐induced cells. MiR‐222‐3p inhibitor reversed the antagonistic effect of Tectorigenin on Dex. The study demonstrates that Tectorigenin inhibits apoptosis of Dex‐induced 9HTE cells by up‐regulating the expression of miR‐222‐3p, which involves with the MAPK pathway.
Glucocorticoids (GCs) can effectively control airway inflammation, but can also cause airway epithelial injury. Tectorigenin, a type of isoflavone isolated from various medicinal plants, has hypolipidemic activity, hepatoprotective, and antioxidant effects. We aimed to investigate whether Tectorigenin can repair GCs-induced airway epithelial injury. Airway epithelial cell line (9HTE cells) were treated with dexamethasone (Dex), Tectorigenin, or further transfected, then cell viability, migration, and invasion were examined by Cell Counting Kit (CCK-8), wound healing, and Transwell assays. The expressions of potential miRNAs related to the effect of Tectorigenin were detected by quantitative polymerase chain reaction (qPCR). Expressions of poptosis-related proteins Bcl-2-associated protein-X (Bax), B-cell lymphoma-2 (Bcl-2), Cleaved Caspase-3, and related to Mitorgen-activated protein kinase (MAPK) signaling pathway serine/threonine kinase (Raf1), extracellular signal-regulated kinase kinase 1/2 (MEK1/2), and extracellular signal-regulated kinase 1/2 (ERK1/2) were detected by Western blot. Dex inhibited the cell viability, migration and invasion by promoting Bax and Cleaved Caspase-3 expressions (p <.001) and by inhibiting the expressions of Bcl-2 and miR-222-3p (p <.001). Then, 10 μmol/L Tectorigenin itself did not affect cell viability but could inhibit the effect of Dex on cell viability, migration, and invasion. Tectorigenin up-regulated the expressions of miR-222-3p, Bcl-2, p-Raf1, p-MEK1/2, and p-ERK1/2 (p <.01), but down-regulated the expressions of Bax and Cleaved Caspase-3 (p <.05) in Dex-induced cells. MiR-222-3p inhibitor reversed the antagonistic effect of Tectorigenin on Dex. The study demonstrates that Tectorigenin inhibits apoptosis of Dex-induced 9HTE cells by up-regulating the expression of miR-222-3p, which involves with the MAPK pathway.
Glucocorticoids (GCs) can effectively control airway inflammation, but can also cause airway epithelial injury. Tectorigenin, a type of isoflavone isolated from various medicinal plants, has hypolipidemic activity, hepatoprotective, and antioxidant effects. We aimed to investigate whether Tectorigenin can repair GCs-induced airway epithelial injury. Airway epithelial cell line (9HTE cells) were treated with dexamethasone (Dex), Tectorigenin, or further transfected, then cell viability, migration, and invasion were examined by Cell Counting Kit (CCK-8), wound healing, and Transwell assays. The expressions of potential miRNAs related to the effect of Tectorigenin were detected by quantitative polymerase chain reaction (qPCR). Expressions of poptosis-related proteins Bcl-2-associated protein-X (Bax), B-cell lymphoma-2 (Bcl-2), Cleaved Caspase-3, and related to Mitorgen-activated protein kinase (MAPK) signaling pathway serine/threonine kinase (Raf1), extracellular signal-regulated kinase kinase 1/2 (MEK1/2), and extracellular signal-regulated kinase 1/2 (ERK1/2) were detected by Western blot. Dex inhibited the cell viability, migration and invasion by promoting Bax and Cleaved Caspase-3 expressions (p <.001) and by inhibiting the expressions of Bcl-2 and miR-222-3p (p <.001). Then, 10 μmol/L Tectorigenin itself did not affect cell viability but could inhibit the effect of Dex on cell viability, migration, and invasion. Tectorigenin up-regulated the expressions of miR-222-3p, Bcl-2, p-Raf1, p-MEK1/2, and p-ERK1/2 (p <.01), but down-regulated the expressions of Bax and Cleaved Caspase-3 (p <.05) in Dex-induced cells. MiR-222-3p inhibitor reversed the antagonistic effect of Tectorigenin on Dex. The study demonstrates that Tectorigenin inhibits apoptosis of Dex-induced 9HTE cells by up-regulating the expression of miR-222-3p, which involves with the MAPK pathway.Glucocorticoids (GCs) can effectively control airway inflammation, but can also cause airway epithelial injury. Tectorigenin, a type of isoflavone isolated from various medicinal plants, has hypolipidemic activity, hepatoprotective, and antioxidant effects. We aimed to investigate whether Tectorigenin can repair GCs-induced airway epithelial injury. Airway epithelial cell line (9HTE cells) were treated with dexamethasone (Dex), Tectorigenin, or further transfected, then cell viability, migration, and invasion were examined by Cell Counting Kit (CCK-8), wound healing, and Transwell assays. The expressions of potential miRNAs related to the effect of Tectorigenin were detected by quantitative polymerase chain reaction (qPCR). Expressions of poptosis-related proteins Bcl-2-associated protein-X (Bax), B-cell lymphoma-2 (Bcl-2), Cleaved Caspase-3, and related to Mitorgen-activated protein kinase (MAPK) signaling pathway serine/threonine kinase (Raf1), extracellular signal-regulated kinase kinase 1/2 (MEK1/2), and extracellular signal-regulated kinase 1/2 (ERK1/2) were detected by Western blot. Dex inhibited the cell viability, migration and invasion by promoting Bax and Cleaved Caspase-3 expressions (p <.001) and by inhibiting the expressions of Bcl-2 and miR-222-3p (p <.001). Then, 10 μmol/L Tectorigenin itself did not affect cell viability but could inhibit the effect of Dex on cell viability, migration, and invasion. Tectorigenin up-regulated the expressions of miR-222-3p, Bcl-2, p-Raf1, p-MEK1/2, and p-ERK1/2 (p <.01), but down-regulated the expressions of Bax and Cleaved Caspase-3 (p <.05) in Dex-induced cells. MiR-222-3p inhibitor reversed the antagonistic effect of Tectorigenin on Dex. The study demonstrates that Tectorigenin inhibits apoptosis of Dex-induced 9HTE cells by up-regulating the expression of miR-222-3p, which involves with the MAPK pathway.
Author Qian, Xiong
Li, Zongqi
Xiao, Qi
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Keywords airway epithelial injury
miR-222-3p
Tectorigenin
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Notes Xiong Qian and Qi Xiao authors contributed equally to this work.
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Snippet Glucocorticoids (GCs) can effectively control airway inflammation, but can also cause airway epithelial injury. Tectorigenin, a type of isoflavone isolated...
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SubjectTerms airway epithelial injury
Antioxidants
Apoptosis
BAX protein
Caspase
Cell migration
Cell Movement
Cell Proliferation
Cell viability
Cholecystokinin
Dexamethasone
Dexamethasone - pharmacology
Epithelial cells
Epithelial Cells - cytology
Epithelial Cells - drug effects
Epithelium
Extracellular signal-regulated kinase
Glucocorticoids
Herbal medicine
Humans
Hypolipidemic activity
Isoflavones - pharmacology
Kinases
Lymphoma
MAP kinase
Medicinal plants
MicroRNAs - genetics
MicroRNAs - metabolism
miR‐222‐3p
Polymerase chain reaction
Protein-serine/threonine kinase
Proteins
Respiratory tract
Respiratory tract diseases
Signal transduction
Tectorigenin
Wound healing
Title Tectorigenin regulates migration, invasion, and apoptosis in dexamethasone‐induced human airway epithelial cells through up‐regulating miR‐222‐3p
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fddr.21795
https://www.ncbi.nlm.nih.gov/pubmed/33543488
https://www.proquest.com/docview/2596827273
https://www.proquest.com/docview/2487162234
Volume 82
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