The DOI matches its Crossref record; 146 of the 146 references it cites were found in a registry or an index.
JNK signaling in cancer cell survival
Abstract
c‐Jun N‐terminal kinase (JNK) is involved in cancer cell apoptosis; however, emerging evidence indicates that this Janus signaling promotes cancer cell survival. JNK acts synergistically with NF‐κB, JAK/STAT, and other signaling molecules to exert a survival function. JNK positively regulates autophagy to counteract apoptosis, and its effect on autophagy is related to the development of chemotherapeutic resistance. The prosurvival effect of JNK may involve an immune evasion mechanism mediated by transforming growth factor‐β, toll‐like receptors, interferon‐γ, and autophagy, as well as compensatory JNK‐dependent cell proliferation. The present review focuses on recent advances in understanding the prosurvival function of JNK and its role in tumor development and chemoresistance, including a comprehensive analysis of the molecular mechanisms underlying JNK‐mediated cancer cell survival. There is a focus on the specific “Yin and Yang” functions of JNK1 and JNK2 in the regulation of cancer cell survival. We highlight recent advances in our knowledge of the roles of JNK in cancer cell survival, which may provide insight into the distinct functions of JNK in cancer and its potential for cancer therapy.
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In the citing paper
“The JAK/STAT pathway interacts with the RAS/MAPK and NF-κB signaling pathways, forming a complex network of cross-talk that influences various cellular processes, including cell proliferation, survival, and apoptosis.”
From Multiple myeloma: signaling pathways and targeted therapy (2024) · cites this paper as [118]
In the citing paper
“However, the JAK/STAT pathway, through its downstream effector Zfh2, can control the expression of the fos gene and the pro-apoptotic hid gene, thereby promoting cell survival mediated by JNK and inhibiting JNK-induced cell apoptosis [118].”
From Multiple myeloma: signaling pathways and targeted therapy (2024) · cites this paper as [118]
Citations
Cites
3 retracted
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RetractedMihailidou, C., Papakotoulas, P., Papavassiliou, A. G., & Karamouzis, M. V. (2017) · Oncotarget · doi:10.18632/oncotarget.23164 · Cited by 31
RetractedPatterns of somatic mutation in human cancer genomes
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Signal integration by JNK and p38 MAPK pathways in cancer development
Wagner, E. F., & Nebreda, Á. R. (2009) · Nature reviews. Cancer · doi:10.1038/nrc2694 · Cited by 2,635
The STATs of cancer — new molecular targets come of age
Yu, H., & Jove, R. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1275 · Cited by 2,278
Autophagy Is Activated for Cell Survival after Endoplasmic ReticulumStress
Ogata, M., Hino, S.-I., Saito, A., Morikawa, K., Kondo, S., Kanemoto, S., Murakami, T., Taniguchi, M., Tanii, I., Yoshinaga, K., et al. (2006) · Molecular and Cellular Biology · doi:10.1128/mcb.01453-06 · Cited by 1,832
Requirement of JNK for Stress- Induced Activation of the Cytochrome c-Mediated Death Pathway
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TGF-β directly targets cytotoxic T cell functions during tumor evasion of immune surveillance
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JNK1-Mediated Phosphorylation of Bcl-2 Regulates Starvation-Induced Autophagy
Wei, Y., Pattingre, S., Sinha, S., Bassik, M., & Levine, B. (2008) · Molecular Cell · doi:10.1016/j.molcel.2008.06.001 · Cited by 1,329
Cited by
Sorted by citations
The JAK/STAT signaling pathway: from bench to clinic
Hu, X., li, J., Fu, M., Zhao, X., & Wang, W. (2021) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-021-00791-1 · Cited by 2,633
Hypoxia-inducible factors: master regulators of hypoxic tumor immune escape
Wu, Q., Li, Y., Nepovimová, E., Heger, Z., Wu, W., Kuča, K., & Adam, V. (2022) · Journal of Hematology & Oncology · doi:10.1186/s13045-022-01292-6 · Cited by 518
Self-citationHypoxia inhibits ferritinophagy, increases mitochondrial ferritin, and protects from ferroptosis
Fuhrmann, D. C., Mondorf, A. W., Beifuß, J., Jung, M., & Brüne, B. (2020) · Redox Biology · doi:10.1016/j.redox.2020.101670 · Cited by 415
The JNK Signaling Pathway in Inflammatory Skin Disorders and Cancer
Hammouda, M., Ford, A. E., Liu, Y., & Zhang, J. Y. (2020) · Cells · doi:10.3390/cells9040857 · Cited by 296
Selective inhibitors for JNK signalling: a potential targeted therapy in cancer
Wu, Q., Wu, W., Jacevic, V. M., França, T. C. C., Wang, X., & Kuča, K. (2020) · Journal of Enzyme Inhibition and Medicinal Chemistry · doi:10.1080/14756366.2020.1720013 · Cited by 172
Self-citation
Metadata
- Authors
- Wu, Q., Wu, W., Fu, B., Shi, L., Wang, X., & Kuca, K.
- Affiliations
- Nanjing Agricultural University (CN)
- Harvard University (US)
- University of Manchester (GB)
- Huazhong Agricultural University (CN)
- Department of Chemistry Faculty of Science, University of Hradec Kralove Hradec Kralove Czech Republic
- Corresponding author
- Wang, Xu
- Venue
- Medicinal Research Reviews
- Publisher
- Wiley
- Published
- 2019-03-25
- Volume
- 39
- Issue
- 6
- Pages
- 2082-2104
- ISSN
- 0198-6325 (ISSN-L)
- 1098-1128
- OpenAlex
- W2923315793
- Cited by
- 322
- References
- 146
- Citations by year
- 2026: 22 · 2025: 51 · 2024: 68 · 2023: 42 · 2022: 56 · 2021: 43 · 2020: 29 · 2019: 11
- FWCI
- 3.40
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Medicinal Research Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31572575, 31602114)
- China Postdoctoral Science Foundation (2016T90477)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Keywords
- JNK signaling, c-Jun N-terminal kinase, tumor cell survival, apoptosis, NF-κB, JAK/STAT signaling, autophagy, chemoresistance, immune evasion, TGF-beta, Toll-like receptors, interferon-gamma, JNK1, JNK2, carcinogenesis, cell proliferation
- MeSH terms
- Animals, Autophagy, Cell Survival, Humans, Neoplasms, Drug Resistance, Neoplasm, MAP Kinase Signaling System, JNK Mitogen-Activated Protein Kinases
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