Paulsen, KaraBenner, ElizabethAlpay Temiz, NuriOstrander, Julie H.2022-08-292022-08-292022https://hdl.handle.net/11299/241244Faculty advisor: Julie H. OstranderAs of 2021, breast cancer is the most common cause of mortality in 20-50 year old women and accounts for 10.4% of malignancy across all cancers.1 Recurrence and resistance that is more common in cancers that have metastasized is thought to be linked to the potential biomarker proline, glutamic acid, and leucine-rich protein 1 (PELP1), which exhibits elevated expression levels in about 70% of breast cancers.2 Previous studies found that inhibition of cytoplasmic PELP1 target genes PFKFB3 and PFKFB4 led to decreased tumorsphere formation, even in models that exhibited hormone therapy resistance.3 Unpublished preliminary research from the Ostrander lab confirmed overexpression of cytoplasmic PELP1 promotes invasion and migration in ER+ breast cancer. To identify which cyto PELP1-induced signaling pathway contributed to breast cancer invasion, the Ostrander lab sent samples off for Reverse Phase Protein Array (RPPA). In the RPPA, 4 different cell lines were analyzed: pCW without doxycycline (doxy), pCW with doxy, pCW cyto PELP1 without doxy, and pCW cyto with doxy. In this cell line model cyto PELP1 is only expressed in the pCW cyto cells in the presence of doxy. The RPPA heatmap data prompted us to probe for Cyclin E, and PFKFB4, neither of which did not exhibit any significant differences in expression across the 4 cell lines. However, GR was found to be downregulated in the pCW cyto with doxy cells. Looking into the raw RPPA data did not yield any significant results either, as 𝛽-catenin was probed for because of its high fold change values. These results validated the RPPA data, however did not highlight any novel cytoplasmic PELP1 induced signaling pathways that potentially promote breast cancer invasion.enPresentation