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 f7 | Aging
← Back
Research Paper Volume 12, Issue 14 pp 15104—15120

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

class="figure-viewer-img"

Figure 7. Pro-MMP-9 protein expression secondary to STAT5a overexpression and 17-β-Estradiol treatment suggest a hormonal regulation of DCIS progression with this transcription factor. (A) MCF10DCIS.com empty vector and STAT5a overexpressor cells were treated with vehicle (DMSO) or 1nM estradiol for 24 hours. Whole cell lysates (75μg) were used to assess the protein expression of MMP-9. GAPDH was used as a loading control. Western blotting was performed in triplicate on cells derived from 3 independent passages. (B) Using the LI-COR imager, densitometry was used to determine the protein expression of MMP-9 upon normalizing to the loading control. Data are reported as % empty vector. Quantitatively, no significant difference in MMP-9 expression was observed between vehicle-treated empty vector and STAT5a overexpressor cells (NS, p=0.382, n=3). Upon treatment with estrogen, a significant increase in MMP-9 protein expression was observed in STAT5a overexpressor cells compared to empty vector cells (39.1-fold, p<0.001, n=3).