Prolactin synergizes with canonical Wnt signals to drive development of ER+ mammary tumors via activation of the Notch pathway.

ABSTRACT: Prolactin (PRL) cooperates with other factors to orchestrate mammary development and lactation, and is epidemiologically linked to higher risk for breast cancer. However, how PRL collaborates with oncogenes to foster tumorigenesis and influence breast cancer phenotype is not well understood. To understand its interactions with canonical Wnt signals, which elevate mammary stem cell activity, we crossed heterozygous NRL-PRL mice with Apc^Min/+ mice and treated pubertal females with a single dose of mutagen. PRL in the context of Apc^Min/+ fueled a dramatic increase in tumor incidence in nulliparous mice, compared to Apc^Min/+ alone. Although carcinomas in both NRL-PRL/Apc^Min/+ and Apc^Min/+ females acquired a mutation in the remaining wildty

SUBMITTER: O'Leary KA 

PROVIDER: S-EPMC7995738 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature