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Cited by 269Cytokine Signaling Pathways and InteractionsProstate Cancer Treatment and ResearchChemokine receptors and signaling

Interleukin-6 regulation of prostate cancer cell growth.

Culig, Zoran, Steiner, Hannes, Bartsch, Georg, Hobisch, Alfred·2005·Journal of Cellular Biochemistry
DOI 10.1002/jcb.20477
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Abstract

Interleukin-6 (IL-6) is involved in regulation of immune reaction and cell growth and differentiation. It causes multifunctional responses ranging from inhibition of proliferation to promotion of cell survival. IL-6 effects may depend on experimental conditions such as passage numbers and serum composition. IL-6 signals in target tissues through the receptor that is composed of the ligand-binding and signal-transducing subunits. IL-6 is expressed in benign and malignant prostate tissue and the levels of the cytokine and its receptor increase during prostate carcinogenesis. IL-6 is considered a positive growth factor for most prostate cells. The only exemption seems to be the LNCaP cell line, in which IL-6 causes growth arrest and induces differentiation function. In contrast, IL-6 acts as an autocrine growth factor in the subline LNCaP-IL-6+ established after chronic treatment with IL-6. IL-6 is a candidate for targeted therapy in prostate cancer because of its association with morbidity. Activation of signaling pathways of Janus kinase/signal transducers and activators of transcription factors, mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3-kinase has been reported in various prostate cancer cell lines. IL-6 and the related cytokine oncostatin M induce activation of the androgen receptor (AR) in the absence of androgen. IL-6 is also involved in regulation of vascular endothelial growth factor expression as well as neuroendocrine differentiation in prostate. Anti-IL-6 antibodies showed an inhibitory effect on the PC-3 xenograft. However, the development of this therapy in prostate cancer is in early stages.

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  • IL-6 predominantly stimulates Janus kinase signaling and activation of STAT proteins, especially STAT3; MAPK and phosphatidylinositol-3 kinase activation can also occur depending on context.

    “The predominant effect of IL-6 in many cell types is the stimulation of Janus kinase (JAK) signaling and activation of signal transducers and activators of transcription (STAT) proteins, especially STAT3; however, activation of MAPK and phosphatidylinositol-3 kinase (PI3K) can also occur depending on the context (13)(14)(15).”

    From Minireview: Alternative Activation Pathways for the Androgen Receptor in Prostate Cancer (2011) · cites this paper as [15]

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Authors
Culig, Z., Steiner, H., Bartsch, G., & Hobisch, A.
Affiliations
  • Innsbruck Medical University (AT)
  • Landeskrankenhaus Feldkirch (AT)
Venue
Journal of Cellular Biochemistry
Publisher
Wiley
Published
2005
Volume
95
Issue
3
Pages
497-505
ISSN
  • 0730-2312 (ISSN-L)
  • 1097-4644
DOI
10.1002/jcb.20477
OpenAlex
W2075760937
Cited by
269
References
74
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2023: 5 · 2022: 7 · 2021: 6 · 2020: 4 · 2019: 8 · 2018: 10 · 2017: 11 · 2016: 11 · 2015: 13 · 2014: 13 · 2013: 23 · 2012: 17
FWCI
2.22
Type
journal article
Language
en
Open access
closed
Licence
doi.wiley.com/10.1002/tdm_license_1.1 (tdm, 3895 d)
Locations
  • Journal of Cellular Biochemistry (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
  • Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
Keywords
interleukin-6, prostate cancer, cell growth regulation, IL-6 receptor, autocrine growth factor, LNCaP cells, androgen receptor, oncostatin M, MAPK signaling, PI3K signaling, JAK/STAT signaling, vascular endothelial growth factor, neuroendocrine differentiation, anti-IL-6 antibody, targeted therapy, prostate carcinogenesis
MeSH terms
Animals, Humans, Male, Prostatic Neoplasms, Receptors, Androgen, Interleukin-6, MAP Kinase Signaling System, Cell Line, Tumor

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