ArticleCell cycle (Georgetown, Tex.)2016
Hepatic stellate cell promoted hepatoma cell invasion via the HGF/c-Met signaling pathway regulated by p53.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 48 citations in OpenAlex.
- Targeting HGF/c-MET signaling to regulate the tumor microenvironment: Implications for counteracting tumor immune evasion.Cell communication and signaling : CCS · 2025Review
- Immunosuppressive tumor microenvironment in the progression, metastasis, and therapy of hepatocellular carcinoma: from bench to bedside.Experimental hematology & oncology · 2024Review
- Article
- Pancreatic Cancer Treatment Targeting the HGF/c-MET Pathway: The MEK Inhibitor Trametinib.Cancers · 2024Review
- Linking fatty liver diseases to hepatocellular carcinoma by hepatic stellate cells.Journal of the National Cancer Center · 2024Review
- HGF-mediated elevation of ETV1 facilitates hepatocellular carcinoma metastasis through upregulating PTK2 and c-MET.Journal of experimental & clinical cancer research : CR · 2022Article
- AXL and MET in Hepatocellular Carcinoma: A Systematic Literature Review.Liver cancer · 2022Review
- Activation of p53 After Irradiation Impairs the Regenerative Capacity of the Mouse Liver.Hepatology communications · 2022Article
- Paeoniflorin Inhibits EMT and Angiogenesis in Human GlioblastomaFrontiers in oncology · 2022Article
- Opposing Roles of Wild-type and Mutant p53 in the Process of Epithelial to Mesenchymal Transition.Frontiers in molecular biosciences · 2022Review
- Novel Pyridine Bioisostere of Cabozantinib as a PotentInternational journal of molecular sciences · 2021Article
- MAPK/ERK Signaling Pathway in Hepatocellular Carcinoma.Cancers · 2021Review
- Research advances of secretory proteins in malignant tumors.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2021Article
- GJA1 promotes hepatocellular carcinoma progression by mediating TGF-β-induced activation and the epithelial-mesenchymal transition of hepatic stellate cells.Open medicine (Warsaw, Poland) · 2021Article
- Inhibiting IRE1α-endonuclease activity decreases tumor burden in a mouse model for hepatocellular carcinoma.eLife · 2020Article
- Preclinical evaluation of a novel triple-acting PIM/PI3K/mTOR inhibitor, IBL-302, in breast cancer.Oncogene · 2020Article
- The Function of the HGF/c-Met Axis in Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2020Review
- Correlation the between the regulation of miRNA-1 in c-Met-induced EMT and cervical cancer progression.Oncology letters · 2019Article
- High-Affinity Human Anti-c-Met IgG Conjugated to Oxaliplatin as Targeted Chemotherapy for Hepatocellular Carcinoma.Frontiers in oncology · 2019Article
- Multipotent mesenchymal stromal cells play critical roles in hepatocellular carcinoma initiation, progression and therapy.Molecular cancer · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The biological behaviors of hepatocellular carcinoma (HCC) are complex mainly due to heterogeneity of progressive genetic and epigenetic mutations as well as tumor environment. Hepatocyte growth factor (HGF)/c-Met signaling pathway is regarded to be a prototypical example for stromal-epithelial interactions during developmental morphogenesis, wound healing, organ regeneration and cancer progression. And p53 plays as an important regulator of Met-dependent cell motility and invasion. Present study showed that 2 HCC cell lines, Hep3B and HepG2, displayed different invasive capacity when treated with HGF which was secreted by hepatic stellate cells (HSCs). We found that HGF promoted Hep3B cells invasion and migration as well as epithelial-mesenchymal transition (EMT) occurrence because Hep3B was p53 deficient, which leaded to the c-Met over-expression. Then we found that HGF/c-Met promoted Hep3B cells invasion and migration by upregulating Snail expression. In conclusion, HGF/c-Met signaling is enhanced by loss of p53 expression, resulting in increased ability of invasion and migration by upregulating the expression of Snail.
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.