Abstract 806: Extracellular matrix metalloprotease inducer (EMMPRIN) and CD44 protein complexes are exclusively formed in basal- and normal-like breast cancer cell lines

Extracellular Matrix Metalloprotease Inducer (EMMPRIN) is a multifunctional glycoprotein that is involved in tumor cell invasion and metastasis, and is a predictor for tamoxifen resistance in breast cancer. EMMPRIN is implicated in development of therapy resistance by forming a functional transporter complex through interaction with CD44 and monocarboxylate transporter 4. Presence of EMMPRIN transporter protein complexes may therefore be a better predictor for therapy resistance and a direct target for drugs. In this study, we aimed to identify EMMPRIN-CD44 protein interactions in a large panel of breast cancer cell lines. EMMPRIN-CD44 protein interaction was investigated in a panel of 41 breast cancer cell lines, which represent the luminal (n=12), ErbB2 (n=13), basal (n=7), and normal-like (n=9) intrinsic subtypes, using in situ Proximity Ligation Assay (isPLA). In addition, protein expression of both EMMPRIN and CD44 in the cell lines was evaluated by immunohistochemistry (IHC). IHC and isPLA read-out was performed by bright field microscopy and 0-1-2-3 scoring was applied to none-weak-moderate-strong staining (IHC) or interaction (isPLA), respectively. Moderate and strong EMMPRIN expression was observed in 50% of luminal, 36% of ErbB2, 86% of basal, and 100% of normal-like cell lines, and moderate to high CD44 expression was detected in 64%, 83%, 86%, and 100% in luminal, ErbB2, basal, and normal-like cell lines, respectively. Interestingly, moderate to strong EMMPRIN-CD44 interaction was exclusively detected in basal (64%) and normal-like (67%) cell lines, whereas luminal and ErbB2 cells lines had no detectible, or only very weak, EMMPRIN-CD44 interaction (≥square = 23.5, P Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 806. doi:1538-7445.AM2012-806