ReviewSeminars in cancer biology2018
Protein kinase C as a tumor suppressor.
Review in Seminars in cancer biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed.
- Integrating machine learning and single-cell sequencing to reveal the role of kinase-related genes in subtype classification and prognostic significance of lung squamous cell carcinoma.Discover oncology · 2026Article
- Multi-Omics and Machine Learning Analyses Reveal PIK3CG, PRKCD, and TRIM22 as Potential Markers of Poor Prognosis and Immune Activation in Glioblastoma.Journal of Korean medical science · 2026Article
- Jurkat T-Cell Antigen-Independent Elimination of PMA-Activated Neuroblastoma Cells Is Triggered by CCL2/CCR2, Depends Upon Lipid Raft LFA1/ICAM1 Immune Synapses, Is Mediated by m-TRAIL and Is Augmented by the TrkAIII Oncoprotein.International journal of molecular sciences · 2026Article
- The chordoid gliomaScience signaling · 2025Article
- PMA exerts anti-leukemia effect in PhCancer cell international · 2025Article
- Cochlioquinones 1968-2024: Chemistry, Biosynthesis, and Biological Activities with Future Perspectives.Journal of fungi (Basel, Switzerland) · 2025Review
- Short-Term Intake ofAntioxidants (Basel, Switzerland) · 2025Article
- Revealing Dynamics of Protein Phosphorylation: A Study on the Cashmere Fineness Disparities in Liaoning Cashmere Goats.Molecular biotechnology · 2025Article
- Intracellular Sphingosine-1-Phosphate Induces Lipolysis Through Direct Activation of Protein Kinase C Zeta.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Biased signaling by mutant EGFR underlies dependence on PKCα in lung adenocarcinoma.Cell reports · 2024Article
- PKCActa pharmaceutica Sinica. B · 2024Article
- Extraction optimization and reactivity of 7α-acetoxy-6β-hydroxyroyleanone and ability of its derivatives to modulate PKC isoforms.Scientific reports · 2024Article
- Cancer-associated mutations in protein kinase C theta are loss-of-function.The Biochemical journal · 2024Article
- Article
- Phosphorylation of PP2Ac by PKC is a key regulatory step in the PP2A-switch-dependent AKT dephosphorylation that leads to apoptosis.Cell communication and signaling : CCS · 2024Article
- Quantification of Binding of Small Molecules to Native Proteins Overexpressed in Living Cells.Journal of the American Chemical Society · 2024Article
- Cysteine-rich zinc finger proteins and the nuclear factor kappa-B pathway.Frontiers in chemical biology · 2024Article
- Anticancer activities of natural abietic acid.Frontiers in pharmacology · 2024Review
- An Update on Protein Kinases as Therapeutic Targets-Part I: Protein Kinase C Activation and Its Role in Cancer and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- A Multimodel Study of the Role of Novel PKC Isoforms in the DNA Integrity Checkpoint.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Protein kinase C (PKC) has historically been considered an oncoprotein. This stems in large part from the discovery in the early 1980s that PKC is directly activated by tumor-promoting phorbol esters. Yet three decades of clinical trials using PKC inhibitors in cancer therapies not only failed, but in some cases worsened patient outcome. Why has targeting PKC in cancer eluded successful therapies? Recent studies looking at the disease for insight provide an explanation: cancer-associated mutations in PKC are generally loss-of-function (LOF), supporting an unexpected function as tumor suppressors. And, contrasting with LOF mutations in cancer, germline mutations that enhance the activity of some PKC isozymes are associated with degenerative diseases such as Alzheimer's disease. This review provides a background on the diverse mechanisms that ensure PKC is only active when, where, and for the appropriate duration needed and summarizes recent findings converging on a paradigm reversal: PKC family members generally function by suppressing, rather than promoting, survival signaling.
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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.