ArticleCancer research2010
The c-Jun NH2-terminal kinase 2 plays a dominant role in human epidermal neoplasia.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Histological and Genetic Markers of Cellular Senescence in Keratinocyte Cancers and Actinic Keratosis: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Regulation of cellular senescence in tumor progression and therapeutic targeting: mechanisms and pathways.Molecular cancer · 2025Review
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- Review
- Glycofullerenes Inhibit Particulate Matter Induced Inflammation and Loss of Barrier Proteins in HaCaT Human Keratinocytes.Biomolecules · 2020Article
- Trichohyalin-like 1 protein plays a crucial role in proliferation and anti-apoptosis of normal human keratinocytes and squamous cell carcinoma cells.Cell death discovery · 2020Article
- Review
- Water-Soluble Fullerenol CInternational journal of molecular sciences · 2019Article
- JNK2 Is Required for the Tumorigenic Properties of Melanoma Cells.ACS chemical biology · 2019Article
- Overexpression of PRDM5 promotes acute myeloid leukemia cell proliferation and migration by activating the JNK pathway.Cancer medicine · 2019Article
- Review
- KIND1 Loss Sensitizes Keratinocytes to UV-Induced Inflammatory Response and DNA Damage.The Journal of investigative dermatology · 2017Article
- JNK2 downregulation promotes tumorigenesis and chemoresistance by decreasing p53 stability in bladder cancer.Oncotarget · 2016Article
- PARP14 promotes the Warburg effect in hepatocellular carcinoma by inhibiting JNK1-dependent PKM2 phosphorylation and activation.Nature communications · 2015Article
- Jnk2 deletion disrupts intestinal mucosal homeostasis and maturation by differentially modulating RNA-binding proteins HuR and CUGBP1.American journal of physiology. Cell physiology · 2014Article
- Co-inhibition of NF-κB and JNK is synergistic in TNF-expressing human AML.The Journal of experimental medicine · 2014Article
- The molecular balancing act of p16(INK4a) in cancer and aging.Molecular cancer research : MCR · 2014Review
- JNK signalling in cancer: in need of new, smarter therapeutic targets.British journal of pharmacology · 2014Review
- Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation.PloS one · 2014Article
- JNK is a novel regulator of intercellular adhesion.Tissue barriers · 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
10 authors at 2 institutions in 1 country.
Funding
Abstract
The c-Jun NH(2)-terminal kinase (JNK) signaling cascade has been implicated in a wide range of diseases, including cancer. It is unclear how different JNK proteins contribute to human cancer. Here, we report that JNK2 is activated in more than 70% of human squamous cell carcinoma (SCC) samples and that inhibition of JNK2 pharmacologically or genetically impairs tumorigenesis of human SCC cells. Most importantly, JNK2, but not JNK1, is sufficient to couple with oncogenic Ras to transform primary human epidermal cells into malignancy with features of SCC. JNK2 prevents Ras-induced cell senescence and growth arrest by reducing the expression levels of the cell cycle inhibitor p16 and the activation of NF-kappaB. On the other hand, JNK, along with phosphoinositide 3-kinase, is essential for Ras-induced glycolysis, an energy-producing process known to benefit cancer growth. These data indicate that JNK2 collaborates with other oncogenes, such as Ras, at multiple molecular levels to promote tumorigenesis and hence represents a promising therapeutic target for cancer.
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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.