ArticleCell reports2017
A Role for Mitochondrial Translation in Promotion of Viability in K-Ras Mutant Cells.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 92 citations in OpenAlex.
- Changes in the transcriptome and synthetic lethal dependencies followingProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Selenium Nanoparticles Selectively Target KRAS G13D to Inhibit Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Synthetic lethality in cancer drug discovery: challenges and opportunities.Nature reviews. Drug discovery · 2026Review
- MGANSL: multi-network representation generating with generative adversarial network for synthetic lethality prediction.BMC bioinformatics · 2025Article
- Targeting mitochondrial transporters and metabolic reprogramming for disease treatment.Journal of translational medicine · 2025Review
- Cancer stem cells in meningiomas: novel insights and therapeutic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Targeting KRAS: from metabolic regulation to cancer treatment.Molecular cancer · 2025Review
- A multilineage screen identifies actionable synthetic lethal interactions in human cancers.Nature genetics · 2025Article
- Mitochondrial micro RNAs: Crucial players in carcinogenesis.Oncology research · 2025Review
- Signaling pathways involved in colorectal cancer: pathogenesis and targeted therapy.Signal transduction and targeted therapy · 2024Review
- Regulation of metastatic potential by drug repurposing and mitochondrial targeting in colorectal cancer cells.BMC cancer · 2024Article
- ELISL: early-late integrated synthetic lethality prediction in cancer.Bioinformatics (Oxford, England) · 2024Article
- Guide-specific loss of efficiency and off-target reduction with Cas9 variants.Nucleic acids research · 2023Article
- Review
- Application of CRISPR-Cas9 gene editing technology in basic research, diagnosis and treatment of colon cancer.Frontiers in endocrinology · 2023Review
- Destabilized 3'UTR elements therapeutically degrade ERBB2 mRNA in drug-resistant ERBB2+ cancer models.Frontiers in genetics · 2023Article
- Identifying mutant-specific multi-drug combinations using comparative network reconstruction.iScience · 2022Article
- Metabolic balance in colorectal cancer is maintained by optimal Wnt signaling levels.Molecular systems biology · 2022Article
- Synthetic Vulnerabilities in the KRAS Pathway.Cancers · 2022Review
- Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
Activating mutations in the KRAS oncogene are highly prevalent in tumors, especially those of the colon, lung, and pancreas. To better understand the genetic dependencies that K-Ras mutant cells rely upon for their growth, we employed whole-genome CRISPR loss-of-function screens in two isogenic pairs of cell lines. Since loss of essential genes is uniformly toxic in CRISPR-based screens, we also developed a small hairpin RNA (shRNA) library targeting essential genes. These approaches uncovered a large set of proteins whose loss results in the selective reduction of K-Ras mutant cell growth. Pathway analysis revealed that many of these genes function in the mitochondria. For validation, we generated isogenic pairs of cell lines using CRISPR-based genome engineering, which confirmed the dependency of K-Ras mutant cells on these mitochondrial pathways. Finally, we found that mitochondrial inhibitors reduce the growth of K-Ras mutant tumors in vivo, aiding in the advancement of strategies to target K-Ras-driven malignancy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.