Xiaying Zhao

Main text Jiao D, Sun H, Zhao X, Chen Y, Lv Z, Shi Q, Li Y, Wang C, Gao K. 2024. mTORC1/S6K1 signaling promotes sustained oncogenic translation through modulating CRL3IBTK-mediated ubiquitination of eIF4A1 in cancer cells. eLife 12:RP92236. doi: 10.7554/eLife.92236. Published 13 May 2024 During a recent self-review of our article, we discovered that representative panels in Figure 4F for the cell invasion and migration assays were inadvertently duplicated.

eLife assessment This study reports a novel substrate and a mediator of oncogenesis downstream of mTORC1, a fundamental advance in our understanding of the mechanistic basis of mTORC1-regulated cap-dependent translation and protein synthesis. Using an array of biochemical, proteomic and functional assays, the authors provide compelling evidence for a novel mTORC1/S6K1-IBTK-eIF4A1 signaling axis that promotes cancer pathogenic translation.

Abstract Enhanced protein synthesis is a crucial molecular mechanism that allows cancer cells to survive, proliferate, metastasize, and develop resistance to anti-cancer treatments, and often arises as a consequence of increased signaling flux channeled to mRNA-bearing eukaryotic initiation factor 4F (eIF4F). However, the post-translational regulation of eIF4A1, an ATP-dependent RNA helicase and subunit of the eIF4F complex, is still poorly understood.