Department of Biochemistry Research Lab Publishes Study on how Mortalin Blocks Oncogenic Cell Death
Oncogenic stress can kill cells, yet oncogenic mutations in the kinase BRAF result in enhanced cell survival, often despite the use of targeted inhibitors. In this sequel of cancer research from Dr. Jong-In Park’s lab in Biochemistry Department, Dr. Keith Wu (Instructor of Biochemistry) and colleagues report that a heat shock protein (HSP70)–related chaperone protein called mortalin was critical to blocking a cell death mechanism in BRAF-mutant tumor cells. They found that aberrant activity of the MEK-ERK signaling cascade caused by BRAF mutation promoted a protein-protein interaction that, in the absence of mortalin, induced mitochondrial-mediated cell death. Depleting mortalin or treating cells with HSP70 inhibitor derivatives was cytotoxic selectively to BRAF-mutant tumor cells, including those resistant to the BRAF inhibitor vemurafenib, suggesting that blocking mortalin might be therapeutically effective in BRAF-MEK-ERK pathway–driven tumors.
See the full paper on the ScienceSignaling website.