ArticleActa pharmacologica Sinica2012
Prostanoid EP1 receptor as the target of (-)-epigallocatechin-3-gallate in suppressing hepatocellular carcinoma cells in vitro.
Article in Acta pharmacologica Sinica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 29 citations in OpenAlex.
- Prophylactic and therapeutic effects of aspirin in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Research Progress on the Protective Effect of Green Tea Polyphenol (-)-Epigallocatechin-3-Gallate (EGCG) on the Liver.Nutrients · 2025Review
- Mitoepigenetics pathways and natural compounds: a dual approach to combatting hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2024Review
- The potential of epigallocatechin gallate in the chemoprevention and therapy of hepatocellular carcinoma.Frontiers in pharmacology · 2023Review
- Small Molecule Compounds of Natural Origin Target Cellular Receptors to Inhibit Cancer Development and Progression.International journal of molecular sciences · 2022Review
- Epigallocatechin-3-gallate in the prevention and treatment of hepatocellular carcinoma: experimental findings and translational perspectives.Drug design, development and therapy · 2019Review
- ERα36 is an effective target of epigallocatechin-3-gallate in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2019Article
- Emerging Roles of G Protein-Coupled Receptors in Hepatocellular Carcinoma.International journal of molecular sciences · 2018Review
- A new molecular mechanism underlying the EGCG-mediated autophagic modulation of AFP in HepG2 cells.Cell death & disease · 2017Article
- Prostaglandin E1 protects hepatocytes against endoplasmic reticulum stress-induced apoptosis via protein kinase A-dependent induction of glucose-regulated protein 78 expression.World journal of gastroenterology · 2017Article
- Antitumoral effect of Ocoxin in hepatocellular carcinoma.Oncology letters · 2017Article
- Cyclooxygenase-2 expression is associated with initiation of hepatocellular carcinoma, while prostaglandin receptor-1 expression predicts survival.World journal of gastroenterology · 2016Article
- Article
- Novel Investigations of Flavonoids as Chemopreventive Agents for Hepatocellular Carcinoma.BioMed research international · 2015Review
- Multifaceted roles of PGE2 in inflammation and cancer.Seminars in immunopathology · 2013Review
- Emerging targets in lipid-based therapy.Biochemical pharmacology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the effects of (-)-epigallocatechin-3-gallate (EGCG), an active compound in green tea, on prostaglandin E(2) (PGE(2))-induced proliferation and migration, and the expression of prostanoid EP(1) receptors in hepatocellular carcinoma (HCC) cells.
methodsHCC cell line HepG2, human hepatoma cell lines MHCC-97L, MHCC-97H and human hepatocyte cell line L02 were used. Cell viability was analyzed using MTT assay. PGE(2) production was determined with immunoassay. Wound healing assay and transwell filter assay were employed to assess the extent of HCC cell migration. The expression of EP(1) receptor and Gq protein were examined using Western blot assay.
resultsPGE(2) (4-40000 nmol/L) or the EP(1) receptor agonist ONO-DI-004 (400-4000 nmol/L) increased the viability and migration of HepG2 cells in concentration-dependent manners. EGCG (100 μg/mL) significantly inhibited the viability and migration of HepG2 cells induced by PGE(2) or ONO-DI-004. HepG2 cells secreted an abundant amount of PGE(2) into the medium, and EGCG (100 μg/mL) significantly inhibited the PGE(2)production and EP(1) receptor expression in HepG2 cells. EGCG (100 μg/mL) also inhibited the viability of MHCC-97L cells, but not that of MHCC-97H cells. Both EGCG (100 μg/mL) and EP(1) receptor antagonist ONO-8711 inhibited PGE(2) 4 μmol/L and ONO-DI-004 400 nmol/L-induced growth and migration of HepG2 cells. Both EGCG (100 μg/mL) and ONO-8711 210 nmol/L inhibited PGE(2)- and ONO-DI-004-induced EP(1) expression. EGCG and ONO-8711 had synergistic effects in inhibiting EP(1) receptor expression. PGE(2), ONO-DI-004, ONO-8711, and EGCG had no effects on Gq expression in HepG2 cells, respectively.
conclusionThese findings suggest that the anti-HCC effects of EGCG might be mediated, at least partially, through the suppressing EP(1) receptor expression and PGE(2) production.
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.