Recommend Cancer Biology & Therapy to your librarian for 2008. Download the form here.

Sign up for Table of Contents Alerts.

home subscribe search archive forthcoming

Email this page Print this page

Research Paper

Targeted Inhibition of EG-1 Blocks Breast Tumor Growth

Ming Lu, Maryam R. Sartippour, Liping Zhang, Andrew J. Norris and Mai N. Brooks

volume 6 | issue 6

June 2007


We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:

 Download PDF

If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.

EG-1 is a gene product that is significantly elevated in human breast cancer tissues. Previously, we have shown that EG-1 overexpression stimulates cellular proliferation both in vitro and in vivo. Here, we ask whether this molecule can be targeted for experimental therapeutic purpose. siRNA lentivirus and polyclonal antibody were designed to suppress EG-1 expression. These agents were then used in cell culture proliferation assays and breast tumor xenograft models. Serum and urine from breast cancer patients were also analyzed for the presence of EG-1 peptide. We report here for the first time that endogenous EG-1 can be targeted to inhibit breast tumor growth. This inhibition, whether delivered via siRNA lentivirus or polyclonal antibody, resulted in decreased cellular proliferation in culture and smaller xenografts in mice. The effects were shown in both ER (estrogen receptor)-positive human breast cancer MCF-7 cells, as well as in ER-negative MDA-MB-231 cells. Furthermore, we detected soluble EG-1 in serum and urine of breast cancer patients. These observations demonstrate that EG-1 is relevant to human breast cancer, and is a molecular target worthy of translational efforts into effective breast cancer therapy.




We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:

 Download PDF

If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.