Dehydroeffusol inhibits hypoxia-induced epithelial–mesenchymal transition in non-small cell lung cancer cells through the inactivation of Wnt/β-catenin pathway

Author:

Wei Haitao1,Zhang Feng1,Wang Jiali2,Zhao Min3,Hou Tao1,Li Li4ORCID

Affiliation:

1. Department of Thoracic Surgery, Huaihe Hospital of Henan University, Kaifeng 475000, P.R. China

2. Operating Room, Huaihe Hospital of Henan University, Kaifeng 475000, P.R. China

3. Department of Respiratory, Huaihe Hospital of Henan University, Kaifeng 475000, P.R. China

4. College of Nursing and Health, Henan University, Kaifeng 475001, P.R. China

Abstract

Abstract Dehydroeffusol (DHE) is a phenanthrene compound that possesses anti-tumor activity. However, the effect of DHE on non-small cell lung cancer (NSCLC) has not been investigated previously. Therefore, the objective of our study was to explore the role of DHE in NSCLC and the underlying mechanism. Our results showed that DHE significantly inhibited the cell viability of A549 cells in a dose- and time-dependent manner under normoxic condition. Moreover, A549 cells were more sensitive to DHE under hypoxic condition compared with the A549 cells cultured in normoxic condition. Hypoxia-induced increased migration and invasion abilities were mitigated by DHE in A549 cells. Treatment of DHE caused increased E-cadherin expression and decreased N-cadherin expression in hypoxia-induced A549 cells. DHE also suppressed hypoxia-induced increase in both protein and mRNA levels of hypoxia inducible factor-1α (HIF-1α) expression in A549 cells. Furthermore, DHE inhibited hypoxia-induced activation of Wnt/β-catenin pathway in A549 cells. The inhibitory effect of DHE on hypoxia-induced EMT was reversed by LiCl, which is an activator of Wnt/β-catenin signaling pathway. In conclusion, these findings demonstrated that DHE prevented hypoxia-induced EMT in NSCLC cells by inhibiting the activation of Wnt/β-catenin pathway, suggesting that DHE might serve as a therapeutic target for the NSCLC metastasis.

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry,Biophysics

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