Inhibiting glucose-regulated protein 78 modulates lipid metabolism through controlling stearoyl-CoA desaturase 1

Of the 230,000 new cases of invasive breast cancer diagnosed annually, 70% express the estrogen receptor-α and may be treated with anti-estrogen therapies. While these drugs induce clinical benefit, over 50% will develop resistance. Recently, we have determined a key role of the unfolded protein response endoplasmic reticulum protein chaperone, glucose-regulated protein 78 (GRP78), in mediating anti-estrogen resistance. We now expand the role of GRP78 to include regulation of lipid metabolism.