Figure 2.
Figure 2. Pharmacologic inhibition of HSP90 depletes STK33 and preferentially induces apoptosis in mutant KRAS-dependent cancer cells. (a) Immunoblots of lung cancer (NCI-H520, A549), colon cancer (Caco-2, HCT-116), breast cancer (BT-20, MDA-MB-231), and AML (HL-60, SKM-1) cell lines incubated with increasing concentrations of PU-H71 or 17-AAG for 24 h. (b) Caspase 9 activity in KRAS mutant (mut) and KRAS WT cancer cell lines incubated with 0.5 µM PU-H71 for 24 h. Experiments were done in triplicate. Error bars represent mean ± SEM. One of two independent experiments is shown. (c) Viability and proliferation of mutant KRAS-dependent (mut) and KRAS WT cancer cell lines incubated with low PU-H71 concentrations for 48 h. Experiments were done in triplicate. Error bars represent mean ± SEM. One of two independent experiments is shown.

Pharmacologic inhibition of HSP90 depletes STK33 and preferentially induces apoptosis in mutant KRAS-dependent cancer cells. (a) Immunoblots of lung cancer (NCI-H520, A549), colon cancer (Caco-2, HCT-116), breast cancer (BT-20, MDA-MB-231), and AML (HL-60, SKM-1) cell lines incubated with increasing concentrations of PU-H71 or 17-AAG for 24 h. (b) Caspase 9 activity in KRAS mutant (mut) and KRAS WT cancer cell lines incubated with 0.5 µM PU-H71 for 24 h. Experiments were done in triplicate. Error bars represent mean ± SEM. One of two independent experiments is shown. (c) Viability and proliferation of mutant KRAS-dependent (mut) and KRAS WT cancer cell lines incubated with low PU-H71 concentrations for 48 h. Experiments were done in triplicate. Error bars represent mean ± SEM. One of two independent experiments is shown.

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