ReviewCancer discovery2011
PI3K and STAT3: a new alliance.
Review in Cancer discovery, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 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
80 citing papers in PubMed, 126 citations in OpenAlex.
- Transforming growth factor-β (TGF-β)-mediated connective tissue growth factor (CTGF) expression in hepatic stellate cells requires Stat3 signaling activation.The Journal of biological chemistry · 2013Trial
- Targeting the BMX in cancer: molecular mechanisms and emerging therapeutic strategies.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- PTEN restricts IL-21R signaling in GC B cells and suppresses their differentiation to plasma cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Natural Flavonoid Nobiletin Attenuates Allergic Asthma via Suppression of STAT3/PI3K-AKT and Neutrophil Extracellular Traps.Food science & nutrition · 2025Article
- Fibroblast Activation Protein (FAP)Oncogene · 2025Article
- Double-sided niche regulation in skin stem cell and cancer: mechanisms and clinical applications.Molecular cancer · 2025Review
- Potential bidirectional regulatory effects of botanical drug metabolites on tumors and cardiovascular diseases based on the PI3K/Akt/mTOR pathway.Frontiers in pharmacology · 2025Review
- Inhibition of STAT3: A promising approach to enhancing the efficacy of chemotherapy in medulloblastoma.Translational oncology · 2024Review
- Prevention of Brain Metastases: A New Frontier.Cancers · 2024Review
- Epstein-Barr Virus Latent Membrane Protein 2A (LMP2A) Enhances ATP Production in B Cell Tumors through mTOR and HIF-1α.International journal of molecular sciences · 2024Article
- PQR309, a dual PI3K/mTOR inhibitor, synergizes with gemcitabine by impairing the GSK-3β and STAT3/HSP60 signaling pathways to treat nasopharyngeal carcinoma.Cell death & disease · 2024Article
- Review
- The implications of alternative pre-mRNA splicing in cell signal transduction.Experimental & molecular medicine · 2023Review
- Oncogenic KRAS signaling drives evasion of innate immune surveillance in lung adenocarcinoma by activating CD47.The Journal of clinical investigation · 2023Article
- A pan-cancer analysis of STAT3 expression and genetic alterations in human tumors.Open medicine (Warsaw, Poland) · 2023Article
- STAT3 in tumor fibroblasts promotes an immunosuppressive microenvironment in pancreatic cancer.Life science alliance · 2022Article
- Novel insights for PI3KC3 in mediating lipid accumulation in yellow catfish Pelteobagrus fulvidraco.Fish physiology and biochemistry · 2022Article
- Review
- The synergistic antitumor effect of IL-6 neutralization with NVP-BEZ235 in hepatocellular carcinoma.Cell death & disease · 2022Article
- Wnt and PI3K/Akt/mTOR Survival Pathways as Therapeutic Targets in Glioblastoma.International journal of molecular sciences · 2022Review
20 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
2 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledRecent proteomic data have uncovered an interdependence of PI3K and STAT3. In PI3K-tranformed murine cells, STAT3 is phosphorylated on Y705 and activated in a PI3K-dependent manner. Dominant negative STAT3 interferes with PI3K-induced oncogenic transformation. Phosphorylation of STAT3 in PI3K-transformed murine cells is mediated by the TEC kinase BMX. Observations on glioblastoma stem cells reveal similar critical roles for STAT3 and BMX. The new data document an important role of STAT3 in PI3K-driven oncogenic transformation and mark BMX as a promising therapeutic target that could enhance the effectiveness of PI3K inhibitors. SIGNIFICANCE: The PI3K–TOR and STAT3 signaling pathways represent two distinct regulatory networks. The discovery of a functional link between these pathways is significant for our understanding of PI3K- and STAT3-driven oncogenic mechanisms and identifies the TEC kinase BMX as a new cancer target.
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.