ArticlePloS one2013
Protein kinase R modulates c-Fos and c-Jun signaling to promote proliferation of hepatocellular carcinoma with hepatitis C virus infection.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 47 citations in OpenAlex.
- Ascites reprograms innate lymphoid immune cells in ovarian cancer by promoting ILC2 enrichment and dysfunctional NK-cell states.Journal for immunotherapy of cancer · 2026Article
- Bioinformatics and experimental validation of druggable targets in non-alcoholic fatty liver disease.Scientific reports · 2026Article
- Protein kinase R regulates pancreatic ductal adenocarcinoma progression by modulating the cell cycle via GADD45A.Scientific reports · 2025Article
- Hesperetin Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication by Downregulating the P38/JUN/FOS Pathway In Vitro.Microorganisms · 2025Article
- PKR associates with 4.1R to promote anchorage-independent growth of hepatocellular carcinoma and lead to poor prognosis.Scientific reports · 2024Article
- HSV-1 Triggers an Antiviral Transcriptional Response during Viral Replication That Is Completely Abrogated in PKRPathogens (Basel, Switzerland) · 2023Article
- Regulatory networks driving expression of genes critical for glioblastoma are controlled by the transcription factor c-Jun and the pre-existing epigenetic modifications.Clinical epigenetics · 2023Article
- Analysis of Antioxidant and Antiviral Effects of Olive (Biomolecules · 2023Article
- In Vitro Toxicological Investigation and Risk Assessment of E-Cigarette Aerosols Based on a Novel Solvent-Free Extraction Method.ACS omega · 2022Article
- The diagnostic and prognostic implications of PRKRA expression in HBV-related hepatocellular carcinoma.Infectious agents and cancer · 2022Article
- Article
- The long noncoding RNA of RMRP is downregulated by PERK, which induces apoptosis in hepatocellular carcinoma cells.Scientific reports · 2021Article
- Pulmonary Mesenchymal Stem Cells in Mild Cases of COVID-19 Are Dedicated to Proliferation; In Severe Cases, They Control Inflammation, Make Cell Dispersion, and Tissue Regeneration.Frontiers in immunology · 2021Article
- β-cantenin is potentially involved in the regulation of c-Jun signaling following bovine herpesvirus 1 infection.Veterinary microbiology · 2020Article
- Article
- Article
- DNA hypermethylation of aurora kinase A in hepatitis C virus‑positive hepatocellular carcinoma.Molecular medicine reports · 2019Article
- Stimulated hepatic stellate cell promotes progression of hepatocellular carcinoma due to protein kinase R activation.PloS one · 2019Article
- Roles of protein kinase R in cancer: Potential as a therapeutic target.Cancer science · 2018Review
- Analysis of expression profile data identifies key genes and pathways in hepatocellular carcinoma.Oncology letters · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Double-stranded RNA-activated protein kinase R (PKR) is known to be upregulated by hepatitis C virus (HCV) and overexpressed in hepatocellular carcinoma (HCC). However, the precise roles of PKR in HCC with HCV infection remain unclear. Two HCV replicating cell lines (JFH-1 and H77s), generated by transfection of Huh7.5.1 cells, were used for experiments reported here. PKR expression was modulated with siRNA and a PKR expression plasmid, and cancer-related genes were assessed by real-time PCR and Western blotting; cell lines were further analyzed using a proliferation assay. Modulation of genes by PKR was also assessed in 34 human HCC specimens. Parallel changes in c-Fos and c-Jun gene expression with PKR were observed. Levels of phosphorylated c-Fos and c-Jun were upregulated by an increase of PKR, and were related to levels of phosphorylated JNK1 and Erk1/2. DNA binding activities of c-Fos and c-Jun also correlated with PKR expression, and cell proliferation was dependent on PKR-modulated c-Fos and c-Jun expression. Coordinate expression of c-Jun and PKR was confirmed in human HCC specimens with HCV infection. PKR upregulated c-Fos and c-Jun activities through activation of Erk1/2 and JNK1, respectively. These modulations resulted in HCC cell proliferation with HCV infection. These findings suggest that PKR-related proliferation pathways could be an attractive therapeutic target.
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.