Deficiency of the p53/p63 target Perp alters mammary gland homeostasis and promotes cancer
Abstract
Perp is a transcriptional target of both p53 during DNA damage-induced apoptosis and p63 during stratified epithelial development. Perp-/- mice exhibit postnatal lethality associated with dramatic blistering of the epidermis and oral mucosa, reflecting a critical role in desmosome-mediated intercellular adhesion in keratinocytes. However, the role of Perp in tissue homeostasis in other p63-dependent stratified epithelial tissues is poorly understood. Given that p63 is essential for proper mammary gland development and that cell adhesion is fundamental for ensuring the proper architecture and function of the mammary epithelium, here we investigate Perp function in the mammary gland. Immunofluorescence and Western blot analysis were performed to characterize Perp expression and localization in the mouse mammary epithelium throughout development. The consequences of Perp deficiency for mammary epithelial development and homeostasis were examined by using in vivo mammary transplant assays. Perp protein levels in a variety of human breast cancer cell lines were compared with those in untransformed cells with Western blot analysis. The role of Perp in mouse mammary tumorigenesis was investigated by aging cohorts of K14-Cre/+;p53fl/fl mice that were wild-type or deficient for Perp. Mammary tumor latency was analyzed, and tumor-free survival was assessed using Kaplan-Meier analysis. We show that Perp proteinmore »
- Authors:
-
- Stanford University, CA (United States)
- Lawrence Berkeley National Laboratory (LBNL), Berkeley, CA (United States)
- University of California, Davis, CA (United States)
- Publication Date:
- Research Org.:
- Lawrence Berkeley National Laboratory (LBNL), Berkeley, CA (United States)
- Sponsoring Org.:
- USDOE Office of Science (SC), Biological and Environmental Research (BER); American Cancer Society; Susan G. Komen Foundation; National Institutes of Health (NIH); National Cancer Institute (NCI); USDOD
- OSTI Identifier:
- 1626698
- Grant/Contract Number:
- AC02-05CH11231; PF-08-259-01-CSM; KG080306; K26 RR024037; R37CA064786; U54CA143836; W81XWH0810736; F32CA130365; 5 R01 CA093665-10
- Resource Type:
- Accepted Manuscript
- Journal Name:
- Breast Cancer Research
- Additional Journal Information:
- Journal Volume: 14; Journal Issue: 2; Journal ID: ISSN 1465-542X
- Publisher:
- BioMed Central
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 59 BASIC BIOLOGICAL SCIENCES; oncology; mammary gland; mammary epithelial cell; myoepithelial cell; human breast cancer cell line; mammary epithelium
Citation Formats
Dusek, Rachel L., Bascom, Jamie L., Vogel, Hannes, Baron, Sylvain, Borowsky, Alexander D., Bissell, Mina J., and Attardi, Laura D. Deficiency of the p53/p63 target Perp alters mammary gland homeostasis and promotes cancer. United States: N. p., 2012.
Web. doi:10.1186/bcr3171.
Dusek, Rachel L., Bascom, Jamie L., Vogel, Hannes, Baron, Sylvain, Borowsky, Alexander D., Bissell, Mina J., & Attardi, Laura D. Deficiency of the p53/p63 target Perp alters mammary gland homeostasis and promotes cancer. United States. https://doi.org/10.1186/bcr3171
Dusek, Rachel L., Bascom, Jamie L., Vogel, Hannes, Baron, Sylvain, Borowsky, Alexander D., Bissell, Mina J., and Attardi, Laura D. Fri .
"Deficiency of the p53/p63 target Perp alters mammary gland homeostasis and promotes cancer". United States. https://doi.org/10.1186/bcr3171. https://www.osti.gov/servlets/purl/1626698.
@article{osti_1626698,
title = {Deficiency of the p53/p63 target Perp alters mammary gland homeostasis and promotes cancer},
author = {Dusek, Rachel L. and Bascom, Jamie L. and Vogel, Hannes and Baron, Sylvain and Borowsky, Alexander D. and Bissell, Mina J. and Attardi, Laura D.},
abstractNote = {Perp is a transcriptional target of both p53 during DNA damage-induced apoptosis and p63 during stratified epithelial development. Perp-/- mice exhibit postnatal lethality associated with dramatic blistering of the epidermis and oral mucosa, reflecting a critical role in desmosome-mediated intercellular adhesion in keratinocytes. However, the role of Perp in tissue homeostasis in other p63-dependent stratified epithelial tissues is poorly understood. Given that p63 is essential for proper mammary gland development and that cell adhesion is fundamental for ensuring the proper architecture and function of the mammary epithelium, here we investigate Perp function in the mammary gland. Immunofluorescence and Western blot analysis were performed to characterize Perp expression and localization in the mouse mammary epithelium throughout development. The consequences of Perp deficiency for mammary epithelial development and homeostasis were examined by using in vivo mammary transplant assays. Perp protein levels in a variety of human breast cancer cell lines were compared with those in untransformed cells with Western blot analysis. The role of Perp in mouse mammary tumorigenesis was investigated by aging cohorts of K14-Cre/+;p53fl/fl mice that were wild-type or deficient for Perp. Mammary tumor latency was analyzed, and tumor-free survival was assessed using Kaplan-Meier analysis. We show that Perp protein is expressed in the mammary epithelium, where it colocalizes with desmosomes. Interestingly, although altering desmosomes through genetic inactivation of Perp does not dramatically impair mammary gland ductal development, Perp loss affects mammary epithelial homeostasis by causing the accumulation of inflammatory cells around mature mammary epithelium. Moreover, we show reduced Perp expression in many human breast cancer cell lines compared with untransformed cells. Importantly, Perp deficiency also promotes the development of mouse mammary cancer. Together, these observations demonstrate an important role for Perp in normal mammary tissue function and in mammary cancer suppression. In addition, our findings highlight the importance of desmosomes in cancer suppression and suggest the merit of evaluating Perp as a potential prognostic indicator or molecular target in breast cancer therapy.},
doi = {10.1186/bcr3171},
journal = {Breast Cancer Research},
number = 2,
volume = 14,
place = {United States},
year = {Fri Apr 20 00:00:00 EDT 2012},
month = {Fri Apr 20 00:00:00 EDT 2012}
}
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