ReviewCancer science2016
Glycogen synthase kinase-3β is a pivotal mediator of cancer invasion and resistance to therapy.
Review in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 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
100 citing papers in PubMed, 158 citations in OpenAlex.
- Biological basis and clinical study of glycogen synthase kinase- 3β-targeted therapy by drug repositioning for glioblastoma.Oncotarget · 2017Trial
- A multi-evidence computational and experimental strategy forRSC medicinal chemistry · 2026Article
- Contribution of Mesenchymal-like and Epithelial Cellular Subsets to Chemotherapy Resistance in Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Article
- Searching potential GSK-3β inhibitors from marine sources using atomistic simulations.Molecular diversity · 2026Article
- Network Pharmacology-Based Identification of Potential Targets and Mechanisms of Isoginkgetin in Gastric Cancer.BioMed research international · 2026Article
- GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1.The Journal of clinical investigation · 2025Article
- Contribution of Mesenchymal-like and Epithelial Cellular Subsets to Chemotherapy Resistance in Triple-Negative Breast Cancer.bioRxiv : the preprint server for biology · 2025Article
- The Significance of the Wnt/β-Catenin Pathway and Related Proteins in Gastrointestinal Malignancies.International journal of molecular sciences · 2025Review
- Proteogenomic characterization unveils biomarkers associated with chemoresistance in muscle-invasive bladder cancer.Cell reports. Medicine · 2025Article
- Targeting GSK3β and signaling pathways in breast cancer: role of individual members of miR- 23/24/27 cluster.BMC cancer · 2025Article
- Impact of G1 phase kinetics on the acquisition of stemness in cancer cells: the critical role of cyclin D.Molecular biology reports · 2025Review
- Effect of EMB-FUBINACA on brain endothelial cell angiogenesis: Expression analysis of angiogenic markers.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Article
- GSK3β serves as a novel therapeutic target in patients with type 2 diabetes mellitus complicated by colorectal cancer.American journal of translational research · 2025Article
- NF-κB Transcription Factors: Their Distribution, Family Expansion, Structural Conservation, and Evolution in Animals.International journal of molecular sciences · 2024Article
- GSK3: A potential target and pending issues for treatment of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- The Relationship between Circadian Rhythm and Cancer Disease.International journal of molecular sciences · 2024Review
- GLIMS: A two-stage gradual-learning method for cancer genes prediction using multi-omics data and co-splicing network.iScience · 2024Article
- Lithium downregulates phosphorylated acetyl‑CoA carboxylase 2 and attenuates mitochondrial fatty acid utilization and oxidative stress in cardiomyocytes.Experimental and therapeutic medicine · 2024Article
- Elevated Kallistatin promotes the occurrence and progression of non-alcoholic fatty liver disease.Signal transduction and targeted therapy · 2024Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cell invasion and resistance to therapy are the most intractable biological characteristics of cancer and, therefore, the most challenging for current cancer research and treatment paradigms. Refractory cancers, including pancreatic cancer and glioblastoma, show an inextricable association between the highly invasive behavior of tumor cells and their resistance to chemotherapy, radiotherapy and targeted therapies. These aggressive properties of cancer share distinct cellular pathways that are connected to each other by several molecular hubs. There is increasing evidence to show that glycogen synthase kinase (GSK)-3β is aberrantly activated in various cancer types and this has emerged as a potential therapeutic target. In many but not all cancer types, aberrant GSK3β sustains the survival, immortalization, proliferation and invasion of tumor cells, while also rendering them insensitive or resistant to chemotherapeutic agents and radiation. Here we review studies that describe associations between therapeutic stimuli/resistance and the induction of pro-invasive phenotypes in various cancer types. Such cancers are largely responsive to treatment that targets GSK3β. This review focuses on the role of GSK3β as a molecular hub that connects pathways responsible for tumor invasion and resistance to therapy, thus highlighting its potential as a major cancer therapeutic target. We also discuss the putative involvement of GSK3β in determining tumor cell stemness that underpins both tumor invasion and therapy resistance, leading to intractable and refractory cancer with dismal patient outcomes.
Indexed as
Identifiers
What OpenQuestion holds
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.