التفاصيل البيبلوغرافية
| العنوان: |
Nm23-H1 inhibits hypoxia induced epithelial-mesenchymal transition and stemness in non-small cell lung cancer cells. |
| المؤلفون: |
Wu, Cun-en, Zhuang, Yu-wen, Zhou, Jin-yong, Liu, Shen-lin, Zou, Xi, Wu, Jian, Wang, Rui-ping, Shu, Peng |
| المصدر: |
Biological Chemistry; May2019, Vol. 400 Issue 6, p765-776, 12p, 4 Color Photographs, 3 Graphs |
| مصطلحات موضوعية: |
NON-small-cell lung carcinoma, CANCER cells, HYPOXEMIA, COBALT chloride, CELL differentiation, WNT proteins, CATENINS, CELLULAR signal transduction |
| مستخلص: |
The Nm23 gene has been acknowledged to play a crucial role in lung cancer metastasis inhibitory cascades controlled by multiple factors. Low expression or allelic deletion of nm23-H1 is strongly linked to widespread metastasis and poor differentiation of non-small cell lung cancer (NSCLC). In this study, nm23-H1 was down regulated in epithelial-mesenchymal transition (EMT) and stemness enhancement under cobalt chloride (CoCl2)-induced hypoxia in NSCLC cells. Moreover, knocking down of nm23-H1 by shRNA apparently promoted hypoxia induced EMT and stemness, which was entirely suppressed via over expression of nm23-H1. Mechanistically, the Wnt/β-catenin signaling pathway was found to participate in the nm23-H1-mediated process. Besides, XAV939 prohibited cell EMT and stemness which could be impaired by knocking down of nm23-H1, while stable transfection of nm23-H1 attenuated hypoxia phonotype induced by lithium chloride (LiCl). Generally, our experiment provided evidence that nm23-H1 can reverse hypoxia induced EMT and stemness through the inhibition of the Wnt/β-catenin pathway, which may furnish a deeper perspective into the better treatment or prognosis for NSCLC. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
