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. Author manuscript; available in PMC: 2021 Jan 1.
Published in final edited form as: Mol Cancer Ther. 2020 May 19;19(7):1562–1571. doi: 10.1158/1535-7163.MCT-19-1036

Figure 2. Effects of knocking out PI3K/mTOR TSGs on the dependency of PI3K/mTOR signaling on EGFR activity in HNSCC cells.

Figure 2.

(A) HNSCC cell lines were treated with control non-targeting (NT) or EGFR-siRNA under serum starvation. Cell lysates were analyzed for the indicated protein by western blotting. (B) Parental CAL27, and isogenic cells with the indicated gene knockouts were treated with control non-targeting (NT) or EGFR-siRNA under serum starvation. Cell lysates were analyzed for the indicated proteins by western blotting (Left panel). The band density was analyzed and normalized with control siRNA-treated samples. Data were from triplicate experiments (Right Panel). (C) Parental CAL27, and isogenic cells with indicated gene knockout were serum starved overnight, and then treated with 0.1% DMSO or erlotinib (3 μM) for 1h. Cell lysates were analyzed for the indicated proteins by western blot (left panel). The band density was analyzed and normalized with the vehicle control (0.1% DMSO)-treated samples. Data were from triplicate experiments (right Panel).