ArticleProceedings of the National Academy of Sciences of the United States of America2012
STK33 kinase inhibitor BRD-8899 has no effect on KRAS-dependent cancer cell viability.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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.
The trial behind it
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
43 citing papers in PubMed, 93 citations in OpenAlex.
- 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
- Serine/Threonine Kinase 33 as a Novel Target of Bufalin in Treatment of Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Serine/threonine kinase 33 mediates thrombin-induced interleukin-8 release from human lung epithelial cells in severe asthma.Respiratory research · 2025Article
- Identification of YBX2 and TSKS As STK33 Interacting Proteins in Testicular Germ Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Potential promising of synthetic lethality in cancer research and treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- STK33 as the functional substrate of miR-454-3p for suppression and apoptosis in neuroblastoma.Molecules and cells · 2024Article
- Structural basis for FN3K-mediated protein deglycation.Structure (London, England : 1993) · 2024Article
- Reversible male contraception by targeted inhibition of serine/threonine kinase 33.Science (New York, N.Y.) · 2024Article
- Artificial intelligence-driven new drug discovery targeting serine/threonine kinase 33 for cancer treatment.Cancer cell international · 2023Article
- Chronic jetlag accelerates pancreatic neoplasia in conditionalChronobiology international · 2023Article
- Approaches to inhibiting oncogenic K-Ras.Small GTPases · 2021Review
- 9-ING-41, a Small Molecule Inhibitor of GSK-3β, Potentiates the Effects of Chemotherapy on Colorectal Cancer Cells.Frontiers in pharmacology · 2021Article
- Discovering and validating cancer genetic dependencies: approaches and pitfalls.Nature reviews. Genetics · 2020Review
- Development of synthetic lethality in cancer: molecular and cellular classification.Signal transduction and targeted therapy · 2020Review
- RAS Function in cancer cells: translating membrane biology and biochemistry into new therapeutics.The Biochemical journal · 2020Review
- TargetingInternational journal of molecular sciences · 2020Review
- Integration of multiple biological contexts reveals principles of synthetic lethality that affect reproducibility.Nature communications · 2020Article
- High-Complexity shRNA Libraries and PI3 Kinase Inhibition in Cancer: High-Fidelity Synthetic Lethality Predictions.Cell reports · 2019Article
- Chemogenetic interactions in human cancer cells.Computational and structural biotechnology journal · 2019Review
- Therapeutic strategies to target RAS-mutant cancers.Nature reviews. Clinical oncology · 2018Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Approximately 30% of human cancers harbor oncogenic gain-of-function mutations in KRAS. Despite interest in KRAS as a therapeutic target, direct blockade of KRAS function with small molecules has yet to be demonstrated. Based on experiments that lower mRNA levels of protein kinases, KRAS-dependent cancer cells were proposed to have a unique requirement for the serine/threonine kinase STK33. Thus, it was suggested that small-molecule inhibitors of STK33 might have therapeutic benefit in these cancers. Here, we describe the development of selective, low nanomolar inhibitors of STK33's kinase activity. The most potent and selective of these, BRD8899, failed to kill KRAS-dependent cells. While several explanations for this result exist, our data are most consistent with the view that inhibition of STK33's kinase activity does not represent a promising anti-KRAS therapeutic strategy.
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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.