c-MYC Suppresses BIN1 to Release Poly(ADP-Ribose) Polymerase 1: A Mechanism by Which Cancer Cells Acquire Cisplatin Resistance

Slovénie Pyndiah, Satoshi Tanida, Kazi M. Ahmed, Erica K. Cassimere, Chungyoul Choe, Daitoku Sakamuro*

*To whom correspondence should be addressed. E-mail: dsakam{at}lsuhsc.edu

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• Fig. S1. Exogenous BIN1 has a capacity to sensitize the DU145 prostate cancer cell line to cisplatin similar to that of exogenous p53.
• Fig. S2. Depletion of BIN1 renders the SK-MEL-28 melanoma cell line resistant to cisplatin.
• Fig. S3. Depletion of BIN1 renders the LNCaP prostate cancer cell line resistant to doxorubicin.
• Fig. S4. The SK-MEL-28/CDDP-R cell line acquires resistance to doxorubicin and camptothecin.
• Fig. S5. Establishment of SKOV3 ovarian cancer cell lines stably expressing BIN1 or BIN1ΔMBD.
• Fig. S6. In situ immunofluorescence microscopic analysis of BIN1 proteins.
• Fig. S7. BIN1 increases cisplatin sensitivity in an MBD-dependent manner.
• Fig. S8. Clonogenic assay for cisplatin-dependent cytotoxicity in the presence or absence of BIN1.
• Fig. S9. BIN1 and 10058-F4 inhibit c-MYC–mediated transactivation.
• Fig. S10. BIN1 BAR domain is essential for BIN1-PARP1 interaction.
• Fig. S11. Recombinant GST, GST-BIN1, and GST-free BIN1 proteins.
• Fig. S12. Depletion of PARP1 is sufficient to induce G₂-M arrest.
• Fig. S13. Western analysis of endogenous c-MYC abundance in the presence of cisplatin.
• Fig. S14. The INR element at +1 in the BIN1 core promoter is important for c-MYC–mediated BIN1 gene repression.
• Fig. S15. Depletion of MIZ1 decreases BIN1 promoter activity and BIN1 mRNA.
• Fig. S16. 10058-F4 reduces the protein stability and nuclear localization of endogenous c-MYC.
• Fig. S17. ChIP analysis of the BIN1 core promoter sequence with an anti-MIZ1 antibody in Rat1/c-MYC–ER cells.
• Table S1. Chemicals, primary antibodies, and siRNAs (or shRNAs) used in this study.
• Table S2. Oligonucleotides used in this study.
  

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© 2011 American Association for the Advancement of Science