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

• Published in: Cancer letters Vol. 503; pp. 231 - 239
• Main Authors: O'Leary, Kathleen A., Rugowski, Debra E., Shea, Michael P., Sullivan, Ruth, Moser, Amy R., Schuler, Linda A.
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 10.04.2021; Elsevier Limited
• Subjects: Adenomatous polyposis coli; Adenomatous Polyposis Coli Protein - genetics; Age; Animals; APC; Breast cancer; Carcinoma; Cell junctions; Cell Nucleus - metabolism; Cell Proliferation; Epidemiology; Female; Females; Laboratory animals; Lactation; Mammary Neoplasms, Experimental - chemically induced; Mammary Neoplasms, Experimental - genetics; Mammary Neoplasms, Experimental - pathology; Mice; Mice, Transgenic; Mutagens - toxicity; Mutation; Notch; Notch1 protein; Phenotypes; Prolactin; Prolactin - genetics; Puberty; Receptors, Notch - metabolism; Stem cells; Tumorigenesis; Tumors; Wnt; Wnt protein; Wnt Signaling Pathway; β-Catenin; Notch; Breast cancer; PRL; ENU; ER; β-catenin; CSC; APC; Prolactin; TCF; Wnt; GSI; WT; BrdU

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 unde...