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. 2019 May;95(5):528–536. doi: 10.1124/mol.118.115162

Fig. 3.

Fig. 3.

Responses to HS-173 + ERBB inhibitor treatment in PIK3CA mutant HNSCC cells. (A) HSC-2 cells were treated with increasing concentrations of PI3Kα inhibitor HS-173 and/or EGFR inhibitor gefitinib for 72 hours. Cell viability was measured using a resazurin cell viability assay. Each point is the mean and S.D. of quadruplicate determinations from a single experiment. Each experiment was repeated independently at least three times with similar combination effects; representative data are shown along with analysis using Combenefit software (Di Veroli et al., 2016). (B) Detroit 562 cells were treated with increasing concentrations of PI3Kα inhibitor HS-173 and/or EGFR gefitinib, ERBB2 inhibitor CP-724714, and/or EGFR/ERBB2 inhibitor afatinib for 72 hours. Cell viability was measured using a resazurin cell viability assay. Each point is the mean and S.D. of quadruplicate determinations from a single experiment. This experiment was repeated independently three times with similar combination effects; representative data are shown. (C) Western blot analysis of phosphorylated and total ERBB2 expression after treatment with vehicle (DMSO) or 15- or 60-minute treatment with either ERBB2-specific inhibitor CP-724714 or EGFR/ERBB2 inhibitor afatinib in Detroit 562 cells. HSP90 was used as a loading control.