ArticleScientific reports2016
Activation of c-Jun predicts a poor response to sorafenib in hepatocellular carcinoma: Preliminary Clinical Evidence.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
- Liver cancer development driven by the AP-1/c-Jun~Fra-2 dimer through c-Myc.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Transcriptional regulation of NDUFA4L2 by NFIB induces sorafenib resistance by decreasing reactive oxygen species in hepatocellular carcinoma.Cancer science · 2023Article
- Article
- System XFrontiers in pharmacology · 2022Review
- Investigation of Anti-Liver Cancer Activity of the Herbal Drug FDY003 Using Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Percentage genome change and chromosome 7q amplification predict sorafenib response in advanced hepatocellular carcinoma.Biomedical journal · 2021Article
- Strategies to improve sorafenib efficacy during image-guided treatment of hepatocellular carcinoma.Annals of translational medicine · 2021Review
- Dual Targeting of Sorafenib-Resistant HCC-Derived Cancer Stem Cells.Current oncology (Toronto, Ont.) · 2021Article
- Gene networks and transcriptional regulators associated with liver cancer development and progression.BMC medical genomics · 2021Article
- Effect of the Hypoxia Inducible Factor on Sorafenib Resistance of Hepatocellular Carcinoma.Frontiers in oncology · 2021Review
- Activation of FcRn Mediates a Primary Resistance Response to Sorafenib in Hepatocellular Carcinoma by Single-Cell RNA Sequencing.Frontiers in pharmacology · 2021Article
- The Effect of Alpha Mangostin on Epithelial-Mesenchymal Transition on Human Hepatocellular Carcinoma HepG2 Cells Surviving Sorafenib via TGF-β/Smad Pathways.Advanced pharmaceutical bulletin · 2020Article
- Hepatocellular carcinomas: evolution to sorafenib resistance through hepatic leukaemia factor.Gut · 2019Article
- Diclofenac Potentiates Sorafenib-Based Treatments of Hepatocellular Carcinoma by Enhancing Oxidative Stress.Cancers · 2019Article
- Identification of key genes and pathways in meningioma by bioinformatics analysis.Oncology letters · 2018Article
- Targeting EP4 downstream c-Jun through ERK1/2-mediated reduction of DNMT1 reveals novel mechanism of solamargine-inhibited growth of lung cancer cells.Journal of cellular and molecular medicine · 2017Article
- Overexpression of c-Jun contributes to sorafenib resistance in human hepatoma cell lines.PloS one · 2017Article
- Hepatocellular Carcinoma: Etiology and Current and Future Drugs.Journal of clinical and experimental hepatologyReview
- c-Jun and Fra-2 pair up to Myc-anistically drive HCC.Cell cycle (Georgetown, Tex.)Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We determined the mitogen-activated protein kinase (MAPK) gene expression profile of acquired resistance in sorafenib-sensitive hepatocellular carcinoma (HCC) cells and aimed to identify c-Jun as an important molecule mediating the efficacy of sorafenib. Differences in gene expression of the MAPK signaling between untreated and sorafenib-treated HCC cell lines were investigated using real-time polymerase chain reaction array. Western blot and real-time PCR further evaluated the expression of c-Jun. Pathological specimens from 50 patients with advanced HCC were collected to measure p-c-Jun expression. Sorafenib-resistant HCC cells demonstrated greater levels of basal c-Jun mRNA and protein compared with sorafenib-sensitive HCC cells. Sorafenib activated p-c-Jun in a dose- and time-dependent manner in PLC/PRF/5 and MHCC97H cell lines. Decreased expression levels of 6 genes after sorafenib treatment suggested a robust inhibitory impact of sorafenib on MAPK signaling in HCC cells. c-Jun and p-c-Jun expression levels were inversely correlated with the efficacy of sorafenib; a high expression level of p-c-Jun was associated with resistance to sorafenib and poor overall survival in patients with clinical HCC. p-c-Jun may act as a biomarker for predicting responses of sorafenib treatment, thus advocating targeting of JNK/c-Jun signaling as an optimal therapeutic strategy in a subset of HCC.
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