Lapatinib resistance in HCT116 cells is mediated by elevated MCL-1 expression, decreased BAK activation, and not by ERBB receptor mutation

Data Supplement

Files in this Data Supplement:

• Data Supplement - Figure S1. Lapatinib blocks radiation-induced activation of ERBB1, ERBB2, ERBB3 and activation of ERK1/2 and AKT in HCT116 cells.

  Figure S2 The generation of Lapatinib resistant HCT116 cells: resistance in the presence of serum.

  Figure S3 The generation of Lapatinib resistant HCT116 cells: resistance in MTT assays.

  Figure S4. The cross-resistance of Lapatinib resistant cells to UCN-01 or VP-16.

  Figure S5. The cross-resistance of Lapatinib resistant cells to Taxotere or Oxaliplatinum.

  Figure S6. The cross-resistance of Lapatinib resistant cells to Doxorubicin.

  Figure S7. The expression of drug efflux pumps in parental and Lapatinib adapted HCT116 cells.

  Figure S8. Expression of dominant negative MEK1 and dominant negative AKT does not revert Lapatinib adapted HCT116 cells.

  Figure S9. Expression of dominant negative STAT3 or dominant negative I&kappaB suppresses transcriptional activity from their respective
  promoters in parental and Lapatinib adapted HCT116 cells.

  Figure S10. The expression/phosphorylation of STAT3 and NF B p65 is unaltered comparing parental and Lapatinib adapted HCT116 cells.

  Figure S11. Serum-starvation �induced killing in parental HCT116 cells in the absence of Lapatinib is suppressed by caspase inhibitors.