ArticleGenes & development2016
Functional genomics reveals that tumors with activating phosphoinositide 3-kinase mutations are dependent on accelerated protein turnover.
Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Protein translation: biological processes and therapeutic strategies for human diseases.Signal transduction and targeted therapy · 2024Review
- Trans-omics analysis of insulin action reveals a cell growth subnetwork which co-regulates anabolic processes.iScience · 2022Article
- Frequency of PIK3CA mutations in different subsites of head and neck squamous cell carcinoma in southern Thailand.Journal of pathology and translational medicine · 2022Article
- Interspecies analysis of MYC targets identifies tRNA synthetases as mediators of growth and survival in MYC-overexpressing cells.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Whole-exome sequencing reveals novel mutations and epigenetic regulation in hypopharyngeal carcinoma.Oncotarget · 2017Article
- High-throughput RNAi screen for essential genes and drug synergistic combinations in colorectal cancer.Scientific data · 2017Article
- A Role for Mitochondrial Translation in Promotion of Viability in K-Ras Mutant Cells.Cell reports · 2017Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Activating mutations in the phosphoinositide 3-kinase (PI3K) signaling pathway are frequently identified in cancer. To identify pathways that support PI3K oncogenesis, we performed a genome-wide RNAi screen in isogenic cell lines harboring wild-type or mutant PIK3CA to search for PI3K synthetic-lethal (SL) genes. A combined analysis of these results with a meta-analysis of two other large-scale RNAi screening data sets in PI3K mutant cancer cell lines converged on ribosomal protein translation and proteasomal protein degradation as critical nononcogene dependencies for PI3K-driven tumors. Genetic or pharmacologic inhibition of either pathway alone, but not together, selectively killed PI3K mutant tumor cells in an mTOR-dependent manner. The expression of ribosomal and proteasomal components was significantly up-regulated in primary human colorectal tumors harboring PI3K pathway activation. Importantly, a PI3K SL gene signature containing the top hits of the SL genes identified in our meta-analysis robustly predicted overall patient survival in colorectal cancer, especially among patients with tumors with an activated PI3K pathway. These results suggest that disruption of protein turnover homeostasis via ribosome or proteasome inhibition may be a novel treatment strategy for PI3K mutant human tumors.
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