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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The JAK/STAT pathway interacts with the RAS/MAPK and NF-κB signaling pathways, forming a complex network that influences proliferation, survival, and apoptosis.
“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]
The JAK/STAT pathway, through its downstream effector Zfh2, controls expression of the fos gene and the pro-apoptotic hid gene, promoting JNK-mediated cell survival and inhibiting JNK-induced apoptosis.
“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]
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The JAK/STAT signaling pathway: from bench to clinic
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ROS-mediated JNK pathway critically contributes to PFOS-triggered apoptosis in SH-SY5Y cells
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- 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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