Supplementary Material for:

Targeting the XPO1-dependent nuclear export of E2F7 reverses anthracycline resistance in head and neck squamous cell carcinomas

Natalia Saenz-Ponce, Rachael Pillay, Lilia Merida de Long, Trinayan Kashyap, Christian Argueta, Yosef Landesman, Mehlika Hazar-Rethinam, Samuel Boros, Benedict Panizza, Maarten Jacquemyn, Dirk Daelemans, Orla M. Gannon, Nicholas A. Saunders*

*Corresponding author. Email: nsaunders{at}uq.edu.au

Published 27 June 2018, Sci. Transl. Med. 10, eaar7223 (2018)
DOI: 10.1126/scitranslmed.aar7223

This PDF file includes:

• Fig. S1. SiRNA knockdown of E2F7 and E2F1 is demonstrated in SCC cell lines.
• Fig. S2. E2F1 and E2F7 control SPHK1 mRNA expression.
• Fig. S3. Subcellular localization of survivin, topoisomerase IIa, and p53 is nuclear in SCC cell lines.
• Fig. S4. Subcellular mislocalization of E2F7 is a common defect in prostate, colon, and breast carcinomas.
• Fig. S5. E2F7 is an XPO1 cargo protein.
• Fig. S6. Mislocalization of E2F7 drives anthracycline resistance.
• Fig. S7. Selinexor does not enhance the cytotoxic effect of paclitaxel in SCC25 cells.
• Fig. S8. E2F7 mislocalization is an actionable pathology in HNSCC. Table S1. SiRNA sequences used in this study.
• Reference (48)

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