Aspartyl Aminopeptidase Suppresses Proliferation, Invasion, and Stemness of Breast Cancer Cells via Targeting CD44

5Citations
Citations of this article
8Readers
Mendeley users who have this article in their library.

Abstract

Although involved in diverse cancer processes, the function of aspartyl aminopeptidase (DNPEP) in breast cancer remains elusive. Here, we reported that DNPEP is significantly downregulated in breast cancer tissues. Overexpression of DNPEP resulted in decreased breast cancer cells proliferation, migration, and invasion, while DNPEP knockdown had the opposite effect. Interestingly, we showed that the reduced DNPEP levels were correlated with the elevated cluster of differentiation 44 (CD44) levels in breast cancer. DNPEP promoted CD44 ubiquitin-proteasome-independent degradation, which is dependent on the hydrolase activity of DNPEP. Ectopic DNPEP expression significantly suppressed the stemness properties of breast cancer cells. These results shed light on the prospect of DNPEP in manipulating breast cancer progression. Anat Rec, 302:2178–2185, 2019. © 2019 American Association for Anatomy.

Cite

CITATION STYLE

APA

Geng, N., Zhang, W., Li, Y., & Li, F. (2019). Aspartyl Aminopeptidase Suppresses Proliferation, Invasion, and Stemness of Breast Cancer Cells via Targeting CD44. Anatomical Record, 302(12), 2178–2185. https://doi.org/10.1002/ar.24206

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free