Document Type
Article
Publication Date
2006
College/Unit
Eberly College of Arts and Sciences
Department/Program/Center
Microbiology, Immunology, and Cell Biology
Abstract
Background
The amide class compound, 3, 4-dichloropropionanilide (DCPA) is known to affect multiple signaling pathways in lymphocyte and macrophage including the inhibition of NF-κB ability. However, little is known about the effect of DCPA in cancer cells. Hypoxia-inducible factor 1 (HIF-1) regulates the expression of many genes including vascular endothelial growth factor (VEGF), heme oxygenase 1, inducible nitric oxide synthase, aldolase, enolase, and lactate dehydrogenase A. HIF-1 expression is associated with tumorigenesis and angiogenesis.
Methods
We used Transwell assay to study cell migration, and used immunoblotting to study specific protein expression in the cells.
Results
In this report, we demonstrate that DCPA inhibited the migration and proliferation of DU145 and PC-3 prostate cancer cells induced by serum, insulin, and insulin-like growth factor I (IGF-I). We found that DCPA inhibited HIF-1 expression in a subunit-specific manner in these cancer cell lines induced by serum and growth factors, and decreased HIF-1α expression by affecting its protein stability.
Conclusion
DCPA can inhibit prostate cancer cell migration, proliferation, and HIF-1α expression, suggesting that DCPA could be potentially used for therapeutic purpose for prostate cancer in the future.
Digital Commons Citation
Jiang, Bing-Hua; Liu, Ling-Zhi; Schafer, Rosana; Flynn, Daniel C.; and Barnett, John B., "A novel role for 3, 4-dichloropropionanilide (DCPA) in the inhibition of prostate cancer cell migration, proliferation, and hypoxia-inducible factor 1alpha expression" (2006). Faculty & Staff Scholarship. 2876.
https://researchrepository.wvu.edu/faculty_publications/2876
Source Citation
Jiang, B., Liu, L., Schafer, R. et al. A novel role for 3, 4-dichloropropionanilide (DCPA) in the inhibition of prostate cancer cell migration, proliferation, and hypoxia-inducible factor 1alpha expression. BMC Cancer 6, 204 (2006). https://doi.org/10.1186/1471-2407-6-204
Comments
© 2006 Jiang et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.