The oncoprotein HBXIP upregulates PDGFB via activating transcription factor Sp1 to promote the proliferation of breast cancer cells.

Abstract

We have reported that the oncoprotein hepatitis B virus X-interacting protein (HBXIP) acts as a novel transcriptional coactivator to promote proliferation and migration of breast cancer cells. Previously, we showed that HBXIP was able to activate nuclear factor-κB (NF-κB) in breast cancer cells. As an oncogene, the platelet-derived growth factor beta polypeptide (PDGFB) plays crucial roles in carcinogenesis. In the present study, we found that both HBXIP and PDGFB were highly expressed in breast cancer cell lines. Interestingly, HBXIP was able to increase transcriptional activity of NF-κB through PDGFB, suggesting that HBXIP is associated with PDGFB in the cells. Moreover, HBXIP was able to upregulate PDGFB at the levels of mRNA, protein and promoter in the cells. Then, we identified that HBXIP stimulated the promoter of PDGFB through activating transcription factor Sp1. In function, HBXIP enhanced the proliferation of breast cancer cells through PDGFB in vitro. Thus, we conclude that HBXIP upregulates PDGFB via activating transcription factor Sp1 to promote proliferation of breast cancer cells.

• Authors: Yingyi Zhang, Yu Zhao, Leilei Li, Yu Shen, Xiaoli Cai, Xiaodong Zhang, Lihong Ye
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 434 Issue 2 Pg. 305-10 (May 03 2013) ISSN: 1090-2104 [Electronic] United States
• PMID: 23537647 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2013 Elsevier Inc. All rights reserved.

Chemical References

• Adaptor Proteins, Signal Transducing
• LAMTOR5 protein, human
• Oncogene Proteins
• RNA, Small Interfering
• Sp1 Transcription Factor
• Luciferases

Topics

• Adaptor Proteins, Signal Transducing (genetics, metabolism)
• Breast Neoplasms (metabolism, pathology)
• Cell Proliferation
• Chromatin Immunoprecipitation
• Cloning, Molecular
• Female
• Gene Expression Regulation, Neoplastic
• Genes, Reporter
• Genes, sis
• Humans
• Luciferases (genetics, metabolism)
• MCF-7 Cells
• Oncogene Proteins (genetics, metabolism)
• Plasmids (genetics, metabolism)
• Promoter Regions, Genetic
• RNA, Small Interfering (genetics, metabolism)
• Sp1 Transcription Factor (genetics, metabolism)
• Transcriptional Activation
• Up-Regulation