Lung Cancer: Lung Cancer II |

Antiflammin-1 Inhibits the TGF-β1-Induced Epithelial-Mesenchymal Transition in A549 Cells Through ERK Pathway FREE TO VIEW

Wei Liu, PhD; Yang Li, PhD; Si-yuan Tang, PhD; Zi-Qiang Luo, PhD
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Central South University, Changsha, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A309. doi:10.1016/j.chest.2016.02.322
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SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: Epithelial to mesenchymal transition (EMT) is a process by which an epithelial cell alters its phenotype to that of a mesenchymal cell and may play a critical role in the lung fibrosis. Antiflammin-1 (AF-1, MQMKKVLDS) is a synthetic nonapeptide with a similar sequence to the conserved sequence of uteroglobin (UG) secreted by lung Clara cells. Studies suggest that it has many biological functions. Our previous studies indicated that AF-1 could suppress the TGF-β1-induced EMT in A549 cells. This report is the first to demonstrate the cell signal pathway of AF-1 in inhibiting TGF-β1 induced EMT in A549 cells.

METHODS: A549 cells were seeded in culture dish and grown for 24 h. Before the experiments, the medium was changed to the incubation medium containing TGF-β1 (5 ng/mL) in the absence or presence of AF-1 (100 μM) and with or without ERK inhibitor (10 μM). Then, cells were cultured for an additional 48 h. After that, cells were lysed in RIPA buffer and the expression of E-cadherin and α-smooth muscle actin (α-SMA) were analyzed by western blot.

RESULTS: The results showed that ERK inhibitor had no effect on TGF-β1 induced EMT in A549 cells. However, the effect of AF-1 was reversed by pretreatment with ERK inhibitor.

CONCLUSIONS: In conclusion, AF-1 can inhibit TGF-β1 induced EMT in A549 cells through ERK pathway.

CLINICAL IMPLICATIONS: To contribute to improve the treatment of the EMT-related diseases.

DISCLOSURE: The following authors have nothing to disclose: Wei Liu, Yang Li, Si-yuan Tang, Zi-Qiang Luo

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