ArticleCell2009
Synthetic lethal interaction between oncogenic KRAS dependency and STK33 suppression in human cancer cells.
Article in Cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 304 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
304 citing papers in PubMed, 1 synthesis or guideline pooled it, 540 citations in OpenAlex.
- Synthetic lethal gene pairs: Experimental approaches and predictive models.Frontiers in genetics · 2022Pooled it
- Longitudinal Liquid Biopsy and Mathematical Modeling of Clonal Evolution Forecast Time to Treatment Failure in the PROSPECT-C Phase II Colorectal Cancer Clinical Trial.Cancer discovery · 2018Trial
- ML281 Does Not Function as an STK33 Inhibitor but Modulates Proliferation and Differentiation of Keratinocytes Derived from Hypertrophic Scars.International journal of molecular sciences · 2026Article
- Changes in the transcriptome and synthetic lethal dependencies followingProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Piceatannol attenuates thoracic aortic aneurysm progression by targeting STK33.Biology direct · 2026Article
- The STK33/mTORC1/S6K1/HIF-1α signalling axis drives glycolysis and progression in pancreatic neuroendocrine tumours.Journal of translational medicine · 2026Article
- Targeting a Glutamic Acid in PDEδ with Fluoromethyl-Aryl Electrophiles Impairs K-Ras Signaling.Journal of medicinal chemistry · 2026Article
- A nucleotide-independent, pan-RAS-targeted DARPin elicits anti-tumor activity in a multimodal manner.Molecular oncology · 2025Article
- Serine/Threonine Kinase 33 as a Novel Target of Bufalin in Treatment of Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Identification of YBX2 and TSKS As STK33 Interacting Proteins in Testicular Germ Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- "Undruggable KRAS": druggable after all.Genes & development · 2025Review
- Advances and Challenges in RAS Signaling Targeted Therapy in Leukemia.Molecular cancer therapeutics · 2025Review
- Role of theFrontiers in oncology · 2025Article
- STK32C as a Therapeutic Target in Colorectal Cancer via HSP90-PI3K/AKT/mTOR Signaling.International journal of biological sciences · 2025Article
- STK33 as the functional substrate of miR-454-3p for suppression and apoptosis in neuroblastoma.Molecules and cells · 2024Article
- Machine-learning and scRNA-Seq-based diagnostic and prognostic models illustrating survival and therapy response of lung adenocarcinoma.Genes and immunity · 2024Article
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- TooManyCellsInteractive: A visualization tool for dynamic exploration of single-cell data.GigaScience · 2024Article
244 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 2 countries.
Funding
Abstract
An alternative to therapeutic targeting of oncogenes is to perform "synthetic lethality" screens for genes that are essential only in the context of specific cancer-causing mutations. We used high-throughput RNA interference (RNAi) to identify synthetic lethal interactions in cancer cells harboring mutant KRAS, the most commonly mutated human oncogene. We find that cells that are dependent on mutant KRAS exhibit sensitivity to suppression of the serine/threonine kinase STK33 irrespective of tissue origin, whereas STK33 is not required by KRAS-independent cells. STK33 promotes cancer cell viability in a kinase activity-dependent manner by regulating the suppression of mitochondrial apoptosis mediated through S6K1-induced inactivation of the death agonist BAD selectively in mutant KRAS-dependent cells. These observations identify STK33 as a target for treatment of mutant KRAS-driven cancers and demonstrate the potential of RNAi screens for discovering functional dependencies created by oncogenic mutations that may enable therapeutic intervention for cancers with "undruggable" genetic alterations.
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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.