The Egr-1 is an immediate early response gene encoding a transcription factor that functions in the regulation of cell growth, differentiation, and apoptosis. Estrogen has diverse physiological effects, including cellular proliferation and neuroprotection against brain injury. There are two types of estrogen receptors (ERs), $ER{alpha}$ and $ER{eta}$. $ER{alpha}$-induced Egr-1 expression has been extensively studied; however, the role of $ER{eta}$ is yet not known. In the present study, we investigated whether or not $ER{eta}$ induces Egr-1 expression in C6 rat glioma cells, which express $ER{eta}$ but not $ER{alpha}$. Our results show that $ER{eta}$ promoted up-regulation of Egr-1 expression via a non-genomic mechanism involving the Raf/MEK1/Erk/Elk-1 signaling cascade.