ReviewTargeted oncology2016
Role of C-Jun N-terminal Kinase in Hepatocellular Carcinoma Development.
Review in Targeted oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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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.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- Identification of STEAP4, EPC1, and CLEC1B as non-invasive candidate biomarkers for hepatocellular carcinoma using integrated bioinformatics analysis.Biotechnology reports (Amsterdam, Netherlands) · 2026Article
- PLEKHA4 knockdown induces apoptosis in melanoma cells through the MAPK and β‑catenin signaling pathways.Molecular medicine reports · 2025Article
- Baicalin attenuates aflatoxin BMycotoxin research · 2024Article
- Mulberry leaf extract inhibits obesity and protects against diethylnitrosamine-induced hepatocellular carcinoma in rats.Journal of traditional and complementary medicine · 2024Article
- Understanding Gene Involvement in Hepatocellular Carcinoma: Implications for Gene Therapy and Personalized Medicine.Pharmacogenomics and personalized medicine · 2024Review
- Components of the JNK-MAPK pathway play distinct roles in hepatocellular carcinoma.Journal of cancer research and clinical oncology · 2023Article
- Cyclovirobuxine D inhibits growth and progression of non‑small cell lung cancer cells by suppressing the KIF11‑CDC25C‑CDK1‑CyclinB1 GInternational journal of oncology · 2023Article
- Inflammatory factor tumor necrosis factor-α (TNF-α) activates P-glycoprotein (P-gp) by phosphorylating c-Jun and thus promotes transportation in placental cells.Translational pediatrics · 2022Article
- Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma.International journal of molecular sciences · 2022Review
- Ethyl Acetate Fraction ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Article
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- LINC01348 suppresses hepatocellular carcinoma metastasis through inhibition of SF3B3-mediated EZH2 pre-mRNA splicing.Oncogene · 2021Article
- Fatty acid binding protein-4 promotes alcohol-dependent hepatosteatosis and hepatocellular carcinoma progression.Translational oncology · 2021Article
- Probing Synergistic Targets by Natural Compounds for Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2021Article
- Anti-cancer potential of persimmon (Diospyros kaki) leaves via the PDGFR-Rac-JNK pathway.Scientific reports · 2020Article
- Long Noncoding RNAs Coregulated by Annexin A7 and JNK in Hepatocellular Carcinoma Cells Identified by Whole-Genome Expression Profiling.BioMed research international · 2020Article
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- Pro-inflammatory TNF-α and IFN-γ Promote Tumor Growth and Metastasis via Induction of MACC1.Frontiers in immunology · 2020Article
- ALDH2 deficiency promotes alcohol-associated liver cancer by activating oncogenic pathways via oxidized DNA-enriched extracellular vesicles.Journal of hepatology · 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is among the most frequently occurring cancers and the leading causes of cancer mortality worldwide. Identification of the signaling pathways regulating liver carcinogenesis is critical for developing novel chemoprevention and targeted therapies. C-Jun N-terminal kinase (JNK) is a member of a larger group of serine/threonine (Ser/Thr) protein kinases known as the mitogen-activated protein kinase (MAPK) family. JNK is an important signaling component that converts external stimuli into a wide range of cellular responses, including cell proliferation, differentiation, survival, migration, invasion, and apoptosis, as well as the development of inflammation, fibrosis, cancer growth, and metabolic diseases. Because of the essential roles of JNK in these cellular functions, deregulated JNK is often found to contribute to the development of HCC. Recently, the functions and molecular mechanisms of JNK in HCC development have been addressed using mouse models and human HCC cell lines. Furthermore, recent studies demonstrate that the activation of JNK by oncogenes can promote the development of cancers by regulating the transforming growth factor (TGF)-β/Smad pathway, which makes the oncogenes/JNK/Smad signaling pathway an attractive target for cancer therapy. Additionally, JNK-targeted therapy has a broad potential for clinical applications. In summary, we are convinced that promising new avenues for the treatment of HCC by targeting JNK are on the horizon, which will undoubtedly lead to better, more effective, and faster therapies in the years to come.
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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.