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. Author manuscript; available in PMC: 2023 Jun 1.
Published in final edited form as: Cancer Lett. 2022 Mar 20;535:215659. doi: 10.1016/j.canlet.2022.215659

Figure 5. AMPK KO cells have an impaired DNA damage response.

Figure 5.

A) γH2AX staining. AMPK KO and Rosa26 control cells were treated with 50 nM doxorubicin for the indicated amount of time and stained for γH2AX. Following staining cells were analyzed by flow cytometry. B) Western blots. AMPK KO and Rosa26 control cells were treated with increasing amounts of doxorubicin for 4 hours and lysates blotted for p53. Actin was used as a loading control. C) Densitometry of triplicate Western blots as done in (B) normalized to actin. D) Western blots. AMPK KO and Rosa26 control cells were treated with increasing amounts of doxorubicin for 4 hours and lysates blotted for p21. Actin was used as a loading control. E) Densitometry of triplicate Western blots as done in (D) normalized to actin. F) Overall survival of AML patients by PRKAA1 expression. AML patients from the TCGA database were analyzed for survival by expression level of PRKAA1. Low PRKAA1 (bottom tertile, blue line), High PRKAA1 (Top 4 tertiles, red line). G) Viability assays. Parental MFL2 cells were treated with the nM amounts of AICAR or doxorubicin (DOX) or both as indicated for 72 hours and viability assessed. *=p value <0.05, **=p value <0.01, ***=p value <0.005, ****=p value <0.001.