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Your search keyword '"phosphatidylinositol 3-kinase/protein kinase b/mammalian target of rapamycin pathway"' showing total 2 results
Start Over Descriptor "phosphatidylinositol 3-kinase/protein kinase b/mammalian target of rapamycin pathway" Topic human lens
2 results on '"phosphatidylinositol 3-kinase/protein kinase b/mammalian target of rapamycin pathway"'

1. TGF-β2 induces epithelial-mesenchymal transition in cultured human lens epithelial cells through activation of the PI3K/Akt/mTOR signaling pathway.

Author

RUI GUO, QIANLI MENG, HAIKE GUO, LIJIA XIAO, XIAOHONG YANG, YING CUI, and YU HUANG

Subjects
*CRYSTALLINE lens, *TRANSFORMING growth factors-beta, *EPITHELIAL cells, *PHOSPHATIDYLINOSITOL 3-kinases, *PROTEIN kinase B, *MTOR protein, *MESENCHYMAL stem cells, *CELL transformation, *PHYSIOLOGY
Abstract

The present study aimed to investigate whether the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway is involved in the transforming growth factor β2 (TGF-β2)-induced epithelial-mesenchymal transition (EMT) in human lens epithelial (HLE) cells. HLEB-3 cells were cultured and stimulated with 10 ng/ml TGF-β2 for 24 h. Western blotting was then performed to analyze the expression levels of connexin 43 and fibronectin, and the activities of Akt and mTOR. Confocal cell immunofluorescence was used to observe the expression of phosphorylated (p)-Akt. The toxicity of 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002) was assessed using a Cell Counting Kit-8 assay, and inhibition investigations were performed using a PI3K inhibitor. The expression of connexin 43 was suppressed and the expression of fibronectin was increased when the cells were stimulated with 10 ng/ml TGF-β2 for 24 h. In addition, Akt and mTOR were activated during TGF-β2 -induced EMT. Treatment of with LY294002 (20 βM) inhibited the activation of Akt and mTOR and effectively prevented TGF-β2-induced EMT in the HLECs. Therefore, the results of the present study indicated that TGF-β2 induces EMT by activating the PI3K/Akt/mTOR signaling pathway in cultured HLECs. [ABSTRACT FROM AUTHOR]

Published
2016
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2. TGF-β2 induces epithelial-mesenchymal transition in cultured human lens epithelial cells through activation of the PI3K/Akt/mTOR signaling pathway

Author

Xiaohong Yang, Rui Guo, Yu Huang, Qianli Meng, Haike Guo, Lijia Xiao, and Ying Cui

Subjects
0301 basic medicine, Cancer Research, Epithelial-Mesenchymal Transition, Morpholines, human lens, Biology, Biochemistry, mTORC2, phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin pathway, 03 medical and health sciences, chemistry.chemical_compound, Transforming Growth Factor beta2, Lens, Crystalline, Genetics, Humans, LY294002, Epithelial–mesenchymal transition, Phosphorylation, Molecular Biology, Protein kinase B, Cell Shape, PI3K/AKT/mTOR pathway, Cells, Cultured, transforming growth factor β2, Cell Death, TOR Serine-Threonine Kinases, RPTOR, Epithelial Cells, Articles, Cell biology, 030104 developmental biology, Oncology, chemistry, Chromones, Molecular Medicine, Signal transduction, Phosphatidylinositol 3-Kinase, Proto-Oncogene Proteins c-akt, Signal Transduction
Abstract

The present study aimed to investigate whether the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway is involved in the transforming growth factor β2 (TGF-β2)-induced epithelial-mesenchymal transition (EMT) in human lens epithelial (HLE) cells. HLEB-3 cells were cultured and stimulated with 10 ng/ml TGF-β2 for 24 h. Western blotting was then performed to analyze the expression levels of connexin 43 and fibronectin, and the activities of Akt and mTOR. Confocal cell immunofluorescence was used to observe the expression of phosphorylated (p)-Akt. The toxicity of 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002) was assessed using a Cell Counting Kit-8 assay, and inhibition investigations were performed using a PI3K inhibitor. The expression of connexin 43 was suppressed and the expression of fibronectin was increased when the cells were stimulated with 10 ng/ml TGF-β2 for 24 h. In addition, Akt and mTOR were activated during TGF-β2-induced EMT. Treatment of with LY294002 (20 µM) inhibited the activation of Akt and mTOR and effectively prevented TGF-β2-induced EMT in the HLECs. Therefore, the results of the present study indicated that TGF-β2 induces EMT by activating the PI3K/Akt/mTOR signaling pathway in cultured HLECs.

Published
2014

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