Estrogen (E2) induced EAAC1 expression with a resistance against H2O2 toxicity.
E2 activated Sphk1 to evoke FGFR–ERK cascade and subsequent EAAC1 synthesis.
GPR30 mediated the downstream events of E2 in regulating EAAC1 expression.
20">This study may reveal new targets or drugs for diseases related to oxidative stress.