Faculty Collaboration Database

Bcl-2 and Bax are differentially expressed in hyperplastic, premalignant, and malignant lesions of mammary carcinogenesis. Cell Growth Differ 2000 Aug;11(8):437-45

Date

08/31/2000

Pubmed ID

10965848

Scopus ID

2-s2.0-0033883688 (requires institutional sign-in at Scopus site)   15 Citations

Abstract

Previously, we found that vorozole (Vz), a nonsteroidal aromatase inhibitor, suppresses the development and progression of mammary tumors in rats. Here we evaluated for the first time the expression of cell death-related proteins Bcl-2 and Bax in hyperplastic, premalignant (carcinoma in situ), or malignant (carcinoma) lesions of mammary carcinogenesis; we also assessed whether these proteins are involved in mediating Vz-induced cell death in tumors. We found that Bcl-2 and Bax were equally expressed in epithelial cells of terminal end buds, ducts, and alveoli. However, in myoepithelial cells, the level of Bax expression was much higher than the level of Bcl-2 expression. Bcl-2 and Bax levels in hyperplastic lesions were similar to those of normal mammary epithelial cells but lower in most carcinomas in situ and carcinomas. In animals with established mammary tumors, Vz induced apoptotic cell death, which was primarily associated with a decrease in Bcl-2 and, to a lesser extent, with a decrease in Bax. These data support the hypothesis that Bcl-2 loss is more potent than Bax gain in regulating apoptotic cell death in mammary tumors.

Author List

Shilkaitis A, Graves J, Mehta RR, Hu L, You M, Lubet R, Steele V, Kelloff G, Christov K

MESH terms used to index this publication - Major topics in bold

Animals
Apoptosis
Aromatase Inhibitors
Carcinoma
Epithelial Cells
Female
Hyperplasia
Mammary Glands, Animal
Mammary Neoplasms, Animal
Precancerous Conditions
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-bcl-2
RNA, Messenger
Rats
Rats, Sprague-Dawley
Triazoles
bcl-2-Associated X Protein