MCF10DCIS.com) promoted their invasion, a process accelerated by estrogen treatment and associated with increased levels of the matrix metalloproteinase-9 (MMP-9) precursor. In sum, our results demonstrate a novel regulatory axis (Cav-1♦STAT5a♦MMP-9) in DCIS that is fully activated by the presence of estrogen. Our sudies suggest to further study phosphorylated STAT5a (Y694) as a potential biomarker to guide and predict outcome of DCIS patient population." name="description"> Essential role of STAT5a in DCIS formation and invasion following estrogen treatment - Figure f3 | Aging
Research Paper Volume 12, Issue 14 pp 15104—15120

Essential role of STAT5a in DCIS formation and invasion following estrogen treatment

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Figure 3.

Proliferating Cell Nuclear Antigen (PCNA) increase in Cav-1 KO DCIS-like lesions secondary to estrogen treatment is inhibited by a homozygous STAT5a deletion. Mammary glands of estrogen-treated WT, Cav-1 KO, and Cav-1/STAT5a dKO mice were immunostained with an antibody recognizing proliferating cell nuclear antigen (PCNA). DAPI was used as a nuclear counterstain. The EVOS FL microscope was used to capture images at 40x objective with the DAPI and Texas Red light cubes (blue: DAPI immunostaining; red: PCNA immunostaining). Qualitatively, mammary glands lacking Cav-1 expression showed elevated PCNA expression upon stimulation with estrogen compared to WT counterparts. A STAT5a deletion in the Cav-1 KO mammary gland diminished PCNA expression to WT levels. For each experimental group, immunofluorescence was performed in triplicate on mammary glands derived from 3 independent mice.