ArticleCancers2014
STAT3 Target Genes Relevant to Human Cancers.
Article in Cancers, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 302 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
302 citing papers in PubMed, 523 citations in OpenAlex.
- Is high-risk neuroblastoma induction chemotherapy possible without G-CSF? A pilot study of safety and treatment delays in the absence of primary prophylactic hematopoietic growth factors.Pediatric blood & cancer · 2020Trial
- Impaired angiogenesis and extracellular matrix metabolism in autosomal-dominant hyper-IgE syndrome.The Journal of clinical investigation · 2020Trial
- Antioxidant and anti-inflammatory effects of the extract from rhizomes ofExperimental and therapeutic medicine · 2026Article
- Quantitative Analysis and Network Pharmacology-Based Profiling of Isolated Metabolites from Swertia purpurascens (D.Don) C.B. Clarke.Journal of separation science · 2026Article
- Peptide Loading Complex in Cancer: From Peptide Translocation, Editing, and Loading into MHC-I to a Potential Therapeutic Target.Current medical science · 2026Review
- TLR9-mediated innate immune signaling contributes to acetaminophen-induced injury in the developing lung.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Integrated Evolutionary and Multi-Omic Analysis of STAT Family Activation Across Solid Tumors.Genes · 2026Article
- STAT3 inhibitor STAT-IN-12 induces apoptosis in mutant-p53 MDA-MB-435 and MDA-MB-231 breast cancer cell lines.Molecular biology reports · 2026Article
- The CHI3L1-neutrophil axis drives immune suppression and breast cancer metastatic dissemination.JCI insight · 2026Article
- Pleiotropic Effects of 3-International journal of molecular sciences · 2026Article
- First-in-child phase I trial of p-STAT3 inhibitor WP1066 in pediatric brain tumor patients.JCI insight · 2026Article
- Mechanisms of transcriptional regulation of CCR5, which is the co-receptor for R5-tropic HIV and is also involved in other disease processes.Biochemical Society transactions · 2026Review
- LMO2 regulates STAT3 localization to the nucleus in breast cancer cells.microPublication biology · 2026Article
- Engineering immunity in osteosarcoma: nanomedicine strategies for overcoming immune evasion.Frontiers in immunology · 2026Review
- Nuclear STAT3 expression is associated with favorable prognosis in papillary thyroid carcinoma.European thyroid journal · 2025Article
- Computational screening and molecular dynamics of natural compounds targeting the SH2 domain of STAT3: a multitarget approach using network pharmacology.Molecular diversity · 2025Article
- Fumarate activates the IL-6/JAK/STAT3 pathway by inhibiting KDM4C-mediated H3K36me3 demethylation in FH-knockdown renal cancer cells.British journal of cancer · 2025Article
- Synergistic Reduction of Breast Cancer Cell Viability and Aggressiveness Through Dual Inhibition of APE1 Redox Function and STAT3 Signaling.Cell biology international · 2025Article
- BRSK2 plays a role in autophagy and cancer cell growth and survival under nutrient deprivation stress via the PIK3C3 pathway.Scientific reports · 2025Article
- Loss ofOncotarget · 2025Article
242 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
Since its discovery, the STAT3 transcription factor has been extensively studied for its function as a transcriptional regulator and its role as a mediator of development, normal physiology, and pathology of many diseases, including cancers. These efforts have uncovered an array of genes that can be positively and negatively regulated by STAT3, alone and in cooperation with other transcription factors. Through regulating gene expression, STAT3 has been demonstrated to play a pivotal role in many cellular processes including oncogenesis, tumor growth and progression, and stemness. Interestingly, recent studies suggest that STAT3 may behave as a tumor suppressor by activating expression of genes known to inhibit tumorigenesis. Additional evidence suggested that STAT3 may elicit opposing effects depending on cellular context and tumor types. These mixed results signify the need for a deeper understanding of STAT3, including its upstream regulators, parallel transcription co-regulators, and downstream target genes. To help facilitate fulfilling this unmet need, this review will be primarily focused on STAT3 downstream target genes that have been validated to associate with tumorigenesis and/or malignant biology of human cancers.
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.