Figure 5
Figure 5. Atorvastatin fails to decrease MYC phosphorylation or induce proliferative arrest in K-Ras (G12D) tumors. (A) Analysis of pERK1/2 and pMYC expression in tumor cells overexpressing MYC together with activated K-Ras (G12D). Tumor cells were treated as described and analyzed by Western blot analysis to assess the state of phosphorylation of ERK1/2 and MYC. (B) Analysis of proliferation of tumor cells overexpressing MYC together with activated K-Ras (G12D). Tumor cells were treated with doxycycline to inactivate MYC and K-Ras (G12D) expression or treated with 10 μM atorvastatin (AT), 100 μM mevalonate (Mev), or 10 μM atorvastatin plus 100 μM mevalonate (AT + Mev). (C) Effect of atorvastatin on cells expressing WT c-Myc or mutant c-Myc (S62A) or c-Myc (T58A). HeLa cells were not infected or infected with adenovirus containing murine Myc (Ad-MycWT) or Myc mutated at S62 (Ad-MycS62A), which prevents Myc phosphorylation and activation, or Myc mutated at T58 (Ad-MycT58A), which prevents dephosphorylation of Myc's activation site. Cells were treated or not treated with atorvastatin (10 μM). Images were acquired as in “Viral infections” (magnification 20×).

Atorvastatin fails to decrease MYC phosphorylation or induce proliferative arrest in K-Ras (G12D) tumors. (A) Analysis of pERK1/2 and pMYC expression in tumor cells overexpressing MYC together with activated K-Ras (G12D). Tumor cells were treated as described and analyzed by Western blot analysis to assess the state of phosphorylation of ERK1/2 and MYC. (B) Analysis of proliferation of tumor cells overexpressing MYC together with activated K-Ras (G12D). Tumor cells were treated with doxycycline to inactivate MYC and K-Ras (G12D) expression or treated with 10 μM atorvastatin (AT), 100 μM mevalonate (Mev), or 10 μM atorvastatin plus 100 μM mevalonate (AT + Mev). (C) Effect of atorvastatin on cells expressing WT c-Myc or mutant c-Myc (S62A) or c-Myc (T58A). HeLa cells were not infected or infected with adenovirus containing murine Myc (Ad-MycWT) or Myc mutated at S62 (Ad-MycS62A), which prevents Myc phosphorylation and activation, or Myc mutated at T58 (Ad-MycT58A), which prevents dephosphorylation of Myc's activation site. Cells were treated or not treated with atorvastatin (10 μM). Images were acquired as in “Viral infections” (magnification 20×).

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