The glucose-regulated protein GRP78 is vital in the development of prostate cancer as it promotes cancer cell proliferation, mediates oncogenic signaling, and protects cancer cells from cell death. Professor Amy Lee and colleagues investigated prostate cancer development in mice in which GRP78 had been inactivated. The PTEN tumor suppressor gene had also been inactivated in the mice, as the loss of PTEN is implicated in the development of many human cancers. Results showed that prostate cancer activation and development resulting from the loss of PTEN was prevented by inactivating GRP78.
According to Professor Lee, the findings have “far-reaching implications” for a wide range of human cancers. She is calling for further research to test the role of GRP78 in other cancers and to develop drugs that inhibit GRP78 as she believes that “anti-GRP78 therapy may open up an entirely new approach to stop human cancer.”
Fu Y, Wey S, Wand M, Ye R, Liao CP, Roy-Burman P, Lee AS. Pten null prostate tumorigenesis and AKT activation are blocked by targeted knockout of ER chaperone GRP78/BiP in prostate epithelium. PNAS Published online before print November 25, 2008. doi:10.1073/pnas.0807691105
News release: Researchers Identify Novel Approach For Suppressing Prostate Cancer Development. University of Southern California Health Sciences. November 23rd 2008.
