91P - PRAME, cell migration and invasion of triple negative breast cancer cells (91P)

Date 08 December 2017
Event ESMO Immuno-Oncology Congress 2017
Session Lunch & Poster Display session
Topics Palliative Care
Supportive and Palliative Care
Presenter Boshra Al-Sulaiti
Citation Annals of Oncology (2017) 28 (suppl_11): xi6-xi29. 10.1093/annonc/mdx711
Authors B. Al-Sulaiti, A. Naser, R. Thomas, G. Al-Khadairi, J. Decock
  • Cancer Research Center, QBRI-HBKU, 5825 - Doha/QA



PRAME was discovered as a tumor-associated antigen in melanoma, capable of eliciting a cellular immune response. Re-expression of PRAME has been found in various cancers, including breast cancer where it is associated with poor prognosis. Given its restricted expression pattern in tumors and its immunogenic nature, PRAME is considered a potential target for immune-based interventions. Very little is known about its function in cancer. Hence, this study aims to investigate its role and potential as a target in triple negative breast cancer, an aggressive subtype of breast cancer.


We manipulated the PRAME expression in the triple negative breast cancer cell line BT549 using siRNA to evaluate the effect of ablation on epithelial-to-mesenchymal transition, cell adhesion, cancer cell migration and invasion.


Silencing of PRAME significantly reduced cell migration as observed in a 40% reduction in wound closure compared to control treated cells. We did not find any significant effect on epithelial-to-mesenchymal transition. PRAME silencing did not change the protein expression and/or localization of the epithelial and mesenchymal markers E-cadherin or vimentin respectively. Nor did we observe collective up- or downregulation of the epithelial-to-mesenchymal transcription factors Snail, Twist and Zeb1. In the absence of PRAME, BT549 cancer cells exhibited a more invasive behavior though Matrigel but not collagen I, accompanied by an increase in MMP-2 and MMP-9. We are currently investigating the effect of PRAME on cell matrix adhesion in order to gain more insight into its role in cell migration and invasion. In addition, we observed enlarged nuclei after PRAME silencing, a well-known characteristic of advanced/metastatic malignancy. Since the mechanisms controlling nuclear size remain unclear, it is of great interest to explore how PRAME is involved in this process and how this affects cellular function.


To conclude, our findings collectively suggest that PRAME may exert different, opposing effects on cell migration and invasion in triple negative breast cancer. This might indicate that PRAME plays different roles in localized versus metastatic disease, requiring a different treatment approach for each disease setting.

Clinical trial identification

Legal entity responsible for the study

Dr Julie Decock




All authors have declared no conflicts of interest.