ReviewFrontiers in oncology2015
STAT3-Mediated Metabolic Reprograming in Cellular Transformation and Implications for Drug Resistance.
Review in Frontiers in oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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.
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Who cites it
75 citing papers in PubMed, 141 citations in OpenAlex.
- Telmisartan enhances anti-PD-1 efficacy in MSS colorectal cancer via modulation of PD-L1 and STAT3 signaling.Translational cancer research · 2026Article
- Moderate downregulation of NDUFA13 promotes cardiomyocytes proliferation and heart regeneration through the glycolysis/c‑Myc/International journal of molecular medicine · 2026Article
- Cancer-associated fibroblasts in the lung cancer microenvironment from multi-dimensional mechanisms to therapeutic strategies.Frontiers in oncology · 2026Review
- Enhancing ferroptosis and inhibiting ABCB1 make the novel aldose reductase inhibitor 5F-E a promising sensitizer in liver cancer.Pharmaceutical science advances · 2025Article
- Curcumin and Resveratrol as Dual Modulators of the STAT3 Pathway in Lung Cancer: A Comprehensive Review.Food science & nutrition · 2025Review
- EZH2 knockout in mice activates STAT3 signalling via STAT3 methylation and modulates ferroptosis in pulpitis-affected dental pulp vascular endothelial cells: A laboratory investigation.International endodontic journal · 2025Article
- Downregulation of MPC1 promotes HCC cell proliferation and metastasis via the STAT3 pathway.Journal of molecular histology · 2025Article
- Effects of SB939 are mediated by STAT3 to inhibit breast cancer cell metastasis-related genes.Oncology letters · 2025Article
- Napabucasin targets resistant triple negative breast cancer through suppressing STAT3 and mitochondrial function.Cancer chemotherapy and pharmacology · 2025Article
- SS18-SSX drives TYK2 expression to activate STAT3/Bcl2 axis, facilitating apoptosis evasion and advancing synovial sarcoma progression.Cell biology and toxicology · 2024Article
- Interleukin-1α as a Potential Prognostic Biomarker in Pancreatic Cancer.Biomedicines · 2024Article
- MCL1 inhibition: a promising approach to augment the efficacy of sorafenib in NSCLC through ferroptosis induction.Cell death discovery · 2024Article
- VISTA promotes the metabolism and differentiation of myeloid-derived suppressor cells by STAT3 and polyamine-dependent mechanisms.Cell reports · 2024Article
- Structural determinants of mitochondrial STAT3 targeting and function.Mitochondrial communications · 2024Article
- Review
- Developments in Genetics: Better Management of Ovarian Cancer Patients.International journal of molecular sciences · 2023Review
- Janus kinase inhibitors are potential therapeutics for amyotrophic lateral sclerosis.Translational neurodegeneration · 2023Review
- Oxidative stress in pituitary neuroendocrine tumors: Affecting the tumor microenvironment and becoming a new target for pituitary neuroendocrine tumor therapy.CNS neuroscience & therapeutics · 2023Review
- DNA 5mC and RNA mCell death and differentiation · 2023Article
- 3D Spheroid Configurations Are Possible Indictors for Evaluating the Pathophysiology of Melanoma Cell Lines.Cells · 2023Article
15 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
No grant is acknowledged in the PubMed record.
Abstract
Signal transducer and activator of transcription (STAT)3 mediates the signaling downstream of cytokine and growth factor receptors, regulating the expression of target genes. It is constitutively phosphorylated on tyrosine (Y-P) in many tumors, where its transcriptional activity can induce a metabolic switch toward aerobic glycolysis and down-regulate mitochondrial activity, a prominent metabolic feature of most cancer cells, correlating with reduced production of ROS, delayed senescence, and protection from apoptosis. STAT3 can, however, also localize to mitochondria, where its serine-phosphorylated (S-P) form preserves mitochondrial oxidative phosphorylation and controls the opening of the mitochondrial permeability transition pore, also promoting survival and resistance to apoptosis in response to specific signals/oncogenes such as RAS. Thus, downstream of different signals, both nuclear, Y-P STAT3, and mitochondrial, S-P STAT3, can act by promoting cell survival and reducing ROS production. Here, we discuss these properties in the light of potential connections between STAT3-driven alterations of mitochondrial metabolism and the development of drug resistance in cancer patients.
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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.