Inhibition of non-small-cell lung cancer cell proliferation by Pbx1
Authors:
Open Access
- 1 October 2014
- journal article
- Vol. 26 (5) , 573-578
Abstract
Lung cancer is one of the most deadly human cancers and continues to be a major unsolved health problem worldwide. Here, we evaluate the function of Pbx1 in the proliferation of non-small-cell lung cancer (NSCLC). In contrast with its known proliferative function, we found that Pbx1 inhibits the proliferation of lung cancer cells. In particular, Pbx1-specific RNA interference resulted in increased proliferation in lung cancer cells. In addition, histone H3 phosphorylation was also increased following inhibition of Pbx1 expression. In contrast, Pbx1 overexpression repressed the proliferation of lung cancer cells and inhibited DNA synthesis. Collectively, our data indicate that Pbx1 inhibits proliferation in lung cancer cells, suggesting a complex role for Pbx1 in modulating the proliferation of cancer cells and making this protein a potential new target for lung cancer therapy.Keywords
This publication has 18 references indexed in Scilit:
- Pbx1 Regulates Self-Renewal of Long-Term Hematopoietic Stem Cells by Maintaining Their QuiescenceCell Stem Cell, 2008
- Hox cofactors in vertebrate developmentDevelopmental Biology, 2006
- Abnormalities of caudal pharyngeal pouch development in Pbx1 knockout mice mimic loss of Hox3 paralogsDevelopmental Biology, 2004
- Genotyping over 100,000 SNPs on a pair of oligonucleotide arraysNature Methods, 2004
- The Competitive Nature of HOXB4-Transduced HSC Is Limited by PBX1Immunity, 2003
- Pbx1 inactivation disrupts pancreas development and in Ipf1-deficient mice promotes diabetes mellitusNature Genetics, 2002
- Aberrant expression of homeobox gene HOXA7 is associated with müllerian-like differentiation of epithelial ovarian tumors and the generation of a specific autologous antibody responseProceedings of the National Academy of Sciences, 2001
- HoxA9-mediated immortalization of myeloid progenitors requires functional interactions with TALE cofactors Pbx and MeisOncogene, 2000
- Cancer statistics, 1999CA: A Cancer Journal for Clinicians, 1999
- The human t(1;19) translocation in pre-B ALL produces multiple nuclear E2A-Pbx1 fusion proteins with differing transforming potentials.Genes & Development, 1991