ReviewHepatic oncology2014
STAT3 in hepatocellular carcinoma: new perspectives.
Review in Hepatic oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 63 citations in OpenAlex.
- Overcoming MDSC-Mediated Immunosuppression in Hepatocellular Carcinoma: From Mechanisms to Novel Immunotherapeutic Approaches.Cancers · 2026Review
- Gene, genetics and genetic medicines in gastroenterology: Current status and its future.World journal of gastroenterology · 2026Review
- JI017 induces cell line specific anticancer effects in hepatocellular carcinoma by suppressing the STAT3 signaling pathway.Molecular biology reports · 2025Article
- The role of inflammation induced by necroptosis in the development of fibrosis and liver cancer in novel knockin mouse models fed a western diet.GeroScience · 2025Article
- Leveraging AI to explore structural contexts of post-translational modifications in drug binding.Journal of cheminformatics · 2025Article
- Leveraging AI to Explore Structural Contexts of Post-Translational Modifications in Drug Binding.bioRxiv : the preprint server for biology · 2025Article
- Exploring the JAK/STAT Signaling Pathway in Hepatocellular Carcinoma: Unraveling Signaling Complexity and Therapeutic Implications.International journal of molecular sciences · 2023Review
- Recent advances in targeting the "undruggable" proteins: from drug discovery to clinical trials.Signal transduction and targeted therapy · 2023Review
- Unlocking the Potential: Novel NSAIDs Hybrids Unleash Chemopreventive Power toward Liver Cancer Cells through Nrf2, NF-κB, and MAPK Signaling Pathways.Molecules (Basel, Switzerland) · 2023Article
- METTL3 and STAT3 form a positive feedback loop to promote cell metastasis in hepatocellular carcinoma.Cell communication and signaling : CCS · 2023Article
- Current and novel approaches in the pharmacological treatment of hepatocellular carcinoma.World journal of gastroenterology · 2023Review
- Deciphering STAT3 signaling potential in hepatocellular carcinoma: tumorigenesis, treatment resistance, and pharmacological significance.Cellular & molecular biology letters · 2023Review
- Effect of Quercetin and Fingolimod, Alone or in Combination, on the Sphingolipid Metabolism in HepG2 Cells.International journal of molecular sciences · 2022Article
- Current strategies and progress for targeting the "undruggable" transcription factors.Acta pharmacologica Sinica · 2022Review
- Suppression of the Proliferation of Huh7 Hepatoma Cells Involving the Downregulation of Mutant p53 Protein and Inactivation of the STAT 3 Pathway with Ailanthoidol.International journal of molecular sciences · 2022Article
- PROX1, a Key Mediator of the Anti-Proliferative Effect of Rapamycin on Hepatocellular Carcinoma Cells.Cells · 2022Article
- 3-Formylchromone Counteracts STAT3 Signaling Pathway by Elevating SHP-2 Expression in Hepatocellular Carcinoma.Biology · 2021Article
- Anti-Hepatocellular Carcinoma Biomolecules: Molecular Targets Insights.International journal of molecular sciences · 2021Review
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Chronic liver damage and inflammation are strong promoters of hepatocellular carcinoma (HCC) formation. HCC cells communicate with inflammatory and stromal cells via cytokine/chemokine signals. These heterotypic interactions inhibit immunologic anticancer activities and promote protumorigenic activities, such as angiogenesis or invasiveness. STAT3 mediates several reciprocal interactions between liver cancer cells and stromal cells and modulates preconditions of tumor formation such as chronic inflammation. Therefore, activation of STAT3 is considered as a tumor-promoting event in HCC formation. However, the oncogenic role of STAT3 in cancers has been challenged by several reports that suggest a tumor-suppressive activity. Here we discuss tumor-promoting and tumor-suppressive effects of cytokine-activated STAT3 in HCC.
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.