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Sci. Signal., 29 March 2011
[DOI: 10.1126/scisignal.2001556]

Supplementary Materials for:

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

This PDF file includes:

  • 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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Citation: S. Pyndiah, S. Tanida, K. M. Ahmed, E. K. Cassimere, C. Choe, D. Sakamuro, c-MYC Suppresses BIN1 to Release Poly(ADP-Ribose) Polymerase 1: A Mechanism by Which Cancer Cells Acquire Cisplatin Resistance. Sci. Signal. 4, ra19 (2011).

© 2011 American Association for the Advancement of Science


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