LKB1/AMPK Pathway and Drug Response in Cancer: A Therapeutic Perspective

Figure 3

LKB1 expression regulates response to oxidative stress induced by prooxidant cytotoxic drugs. Isogenic pairs of H460 and HeLa cells (derived from NSCLC and cervical carcinoma, respectively) differing in LKB1 status and generated as described by Zulato et al. [103] were treated with arsenic trioxide, paclitaxel, or doxorubicin for 48 h. Viability was evaluated by the Sulphorhodamine B assay (for materials and methods, refer to [103]) in cells exposed to increasing concentrations of drugs. For each cell line tested, the IC₅₀ values relative to LKB1^mut and LKB1^wt cells are reported. Results are representative of three independent experiments performed in triplicate (^§, ^§§, and ^§§§ LKB1^wt versus LKB1^mut cells). Results of SRB assay revealed that H460 and HeLa LKB1^wt variants were more resistant than their LKB1^mut counterparts to the drugs tested. NE: not evaluable.