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AKT signaling is modulated by a complex network of regulatory proteins and is commonly deregulated in cancer. Here, we present a dual mechanism of  AKT  regulation by the  ERBB  receptor feedback inhibitor 1 ( ERRFI 1). We show that in cells expressing high levels of  EGFR ,  ERRF 1 inhibits growth and enhances responses to chemotherapy. This is mediated in part through the negative regulation of  AKT  signaling by direct  ERRFI 1‐dependent inhibition of  EGFR . In cells expressing low levels of  EGFR ,  ERRFI 1 positively modulates  AKT  signaling by interfering with the interaction of the inactivating phosphatase  PHLPP  with  AKT , thereby promoting cell growth and chemotherapy desensitization. These observations broaden our understanding of chemotherapy response and have important implications for the selection of targeted therapies in a cell context‐dependent manner.  EGFR  inhibition can only sensitize  EGFR ‐high cells for chemotherapy, while  AKT  inhibition increases chemosensitivity in  EGFR ‐low cells. By understanding these mechanisms, we can take advantage of the cellular context to individualize antineoplastic therapy. Finally, our data also suggest targeting of  EFFRI 1 in  EGFR ‐low cancer as a promising therapeutic approach.

Differential roles of ERRFI1 in EGFR and AKT pathway regulation affect cancer proliferation