Role of the Catenin p120 in Breast Cancer.

摘要

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 pl20 inactivation in breast cancer, we have proposed to study the consequences of targeted p120 loss of function in the mammary glands 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. We report here that the floxed p120 mouse has now been successfully generated. There are three male and two female mice, all of which contain the homologously recombined construct. This was the most difficult hurdle in the project. We can now proceed to target the p120 KO to the mammary gland and study in detail the outcome with respect to normal and cancerous behavior. The mouse will be invaluable for studying further the role of p120 in metastasis and breast cancer.