Role of the Catenin p120 in Breast Cancer
Abstract
Our working hypothesis is that induced p120 loss in the breast will impair E-cadherin function leading to (1) severe adverse consequences to lobular-alveolar development, and (2) positive effects on tumorigenesis or tumor progression leading to increased invasion and metastasis. To determine the role of p120 inactivation in breast cancer, we have proposed to study the consequences of targeted p120 loss of function in the mammary gland of normal and transgenic mouse models for tumorigenesis and metastasis. The first aim proposes to use gene targeting to incorporate loxP sites at strategic locations in the p120 gene such that Cre recombinase-induced deletion of the intervening sequence will inactivate p120. Mice containing this conditional allele (p120fl0X) will be generated and crossed with WAP-Cre mice to target the conditional deletion to the breast. Our major progress in this reporting period is the completion of the targeting construct, a key objective that required sequencing the p120 genomic DNA, inserting lox p sites, and subcloning to the appropriate tranfection vector. Thus, we can now move forward with generation of the p120 knockout mouse. The mouse will be invaluable for studying further the role of p120 in metastasis and breast cancer.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2000
- Accession Number
- ADA387234
Entities
People
- Albert B. Reynolds
Organizations
- Vanderbilt University Medical Center