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Although Sorafenib is a kinase inhibitor with multiple targets including RTKs and RAF, its treatment did not affect the total tyrosyl phosphorylation and ERK phosphorylation in TamR cells (Figure S5), indicating that inhibition of TamR ER+ breast cancer cell growth by Sorafenib under the concentration used is not through inhibition of RTKs and RAF

Context-dependent functional differences among AREs fit with findings from another group that combined high-throughput promoter-dependent drug screens and transcriptomics analyses to uncover that low doses of the chemotherapeutic doxorubicin downregulate cell cycle genes while high doses upregulate DNA damage response genes