ArticlePathology oncology research : POR2017
E
Article in Pathology oncology research : POR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.
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
9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 9 citations in OpenAlex.
- Molecular mechanisms of sex hormones in Hepatocellular Carcinoma: a systematic review.Molecular biology reports · 2025Pooled it
- Intricate roles of estrogen and estrogen receptors in digestive system cancers: a systematic review.Cancer biology & medicine · 2024Pooled it
- Intratumoral but not circulating estradiol predicts postoperative survival in men with hepatocellular carcinoma.Discover oncology · 2026Article
- Sensitization of hepatocellular carcinoma cells to HDACi is regulated through hsa-miR-342-5p/CFL1.Cancer cell international · 2024Article
- Exploiting gender-based biomarkers and drug targets: advancing personalized therapeutic strategies in hepatocellular carcinoma.Frontiers in pharmacology · 2024Review
- Therapeutic Value of Estrogen Receptor α in Hepatocellular Carcinoma Based on Molecular Mechanisms.Journal of clinical and translational hepatology · 2022Review
- Molecular Initiating Events Associated with Drug-Induced Liver Malignant Tumors: An Integrated Study of the FDA Adverse Event Reporting System and Toxicity Predictions.Biomolecules · 2021Article
- Estrogen Receptor 1 Inhibition of Wnt/β-Catenin Signaling Contributes to Sex Differences in Hepatocarcinogenesis.Frontiers in oncology · 2021Article
- Overexpression Of ERβ Participates In The Progression Of Liver Cancer Via Inhibiting The Notch Signaling Pathway.OncoTargets and therapy · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peroxisome proliferator-activated receptor-α (PPARα) is a member of the nuclear receptor superfamily involved in hepatocarcinogenesis in rodents. In previous studies on liver tumor tissues, PPARα mRNA expression was found to be significantly higher and overexpression of ERα inhibited the PPARα expression, cell-proliferation and also induced apoptosis in Hep3B cell. However, the role of ERβ is not known yet. Therefore, the aim of this study is to define the role of ERβ on PPARα in Hep3B cells. The effect of PPARα signaling cascade were monitored by inducing Hep3B cells by fenofibrate. Further the cells were transfected with pCMV-ERβ and the consequences of ERβ-overexpression on the PPARα induced changes such as enhanced cell-proliferation and suppressed apoptosis were determined using western blot analysis and TUNEL assay. The EMSA was used to identify whether ERβ modulates PPARα expression by binding to PPARα promoter region to repress PPARα promoter activity. In addition, the direct interaction between ERβ and PPARα proteins was verified by co-immunoprecipitation assay. Our results show that the overexpressed ERβ not only attenuated the effects of fenofibrate to induce the levels of apoptosis protein such as Cyt.c, Caspase 9 and Caspase 3 but also inhibited the levels of survival protein such Bcl-xL, p-Bad, cyclin A and cyclin E. All these effects of E
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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.