Vemurafenib Potently Induces Endoplasmic Reticulum Stress–Mediated Apoptosis in BRAFV600E Melanoma Cells

Daniela Beck, Heike Niessner, Keiran S. M. Smalley, Keith Flaherty, Kim H. T. Paraiso, Christian Busch, Tobias Sinnberg, Sophie Vasseur, Juan Lucio Iovanna, Stefan Drießen, Björn Stork, Sebastian Wesselborg, Martin Schaller, Tilo Biedermann, Jürgen Bauer, Konstantinos Lasithiotakis, Benjamin Weide, Jürgen Eberle, Birgit Schittek, Dirk Schadendorf, Claus Garbe, Dagmar Kulms, Friedegund Meier*

*To whom correspondence should be addressed. E-mail: friedegund.meier{at}t-online.de

This PDF file includes:

• Fig. S1. The UPR pathway.
• Fig. S2. Vemurafenib induces apoptosis in BRAF-mutant melanoma cells.
• Fig. S3. Caspase inhibition blocks vemurafenib-induced apoptosis in melanoma cells.
• Fig. S4. Vemurafenib does not increase the abundance of GRP78 at early time points.
• Fig. S5. Thapsigargin and tunicamycin do not affect the survival of human fibroblasts at concentrations that induced apoptosis in melanoma cells.
• Fig. S6. Conventional ER stress inducers enhance vemurafenib-induced apoptosis.
• Fig. S7. The HSP90 inhibitor XL888 overcomes intrinsic and acquired vemurafenib resistance.
• Table S1. Mutation analysis of gene sequences in vemurafenib-sensitive and vemurafenib-resistant cell lines.
• Table S2. Forward and reverse primer sequences for quantitative real-time PCR.
• Table S3. Forward and reverse primer sequences for mutation analysis.

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© 2013 American Association for the Advancement of Science