Drs. Li and Cai contributed equally to this work.
Ing4 induces Cell Growth Inhibition in Human Lung Adenocarcinoma A549 Cells by Means of Wnt-1/β-Catenin Signaling Pathway
Article first published online: 9 APR 2008
Copyright © 2008 Wiley-Liss, Inc.
The Anatomical Record
Volume 291, Issue 5, pages 593–600, May 2008
How to Cite
Li, X., Cai, L., Liang, M., Wang, Y., Yang, J. and Zhao, Y. (2008), Ing4 induces Cell Growth Inhibition in Human Lung Adenocarcinoma A549 Cells by Means of Wnt-1/β-Catenin Signaling Pathway. Anat Rec, 291: 593–600. doi: 10.1002/ar.20685
- Issue published online: 9 APR 2008
- Article first published online: 9 APR 2008
- Manuscript Accepted: 5 JAN 2008
- Manuscript Received: 16 JUL 2007
- Special Foundation of Youth Science and Technique of Heilongjiang Province of China. Grant Number: QC07C91
- lung adenocarcinoma;
- Wnt-1/β-catenin signaling
ING4, as a novel candidate tumor suppressor gene, has been implicated in several human malignances by tumor growth inhibition and apoptosis enhancement. The mechanism of ING4 remains largely unknown. The purpose of this study was to investigate the inhibitory tumor growth effects of ING4 on lung adenocarcinoma, and its mechanism, by ING4 cDNA transduction into A549 cells. Furthermore, the expression level of ING4 in lung adenocarcinoma tissues was examined. The expression of ING4 was markedly reduced in human lung adenocarcinoma tissues. Overexpression of ING4 can induce growth inhibition in A549 cells both in vitro and in vivo, and also induce up-regulation of p27, down-regulation of cyclinD1, SKP2, and Cox2, and inactivation of the Wnt-1/β-catenin pathway. Moreover, overexpression of ING4 can enhance the sensitivity of A549 cells to radiotherapy and chemotherapy. Thus, ING4 may play an inhibitory role on A549 cell proliferation and tumor growth in lung adenocarcinoma by up-regulation or down-regulation of cell proliferation-regulating proteins such as p27, cyclinD1, SKP2, and Cox2 by means of inactivation of Wnt-1/β-catenin signaling. Anat Rec, 291:593–600, 2008. © 2008 Wiley-Liss, Inc.