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Cytokines and Janus kinase/signal transducer and activator of transcription signaling in prostate cancer : overview and therapeutic opportunities

Canesin, Giacomo LU ; Krzyzanowska, Agnieszka LU ; Hellsten, Rebecka LU and Bjartell, Anders LU (2020) In Current Opinion in Endocrine and Metabolic Research 10. p.36-42
Abstract

The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway was originally identified as a key cellular mechanism mediating the action of cytokines, interferons, and growth factors for the control of gene expression. Extracellular signals mediated by cytokines are thus transduced through this pathway into transcriptional programs that regulate cell growth, differentiation, proliferation, invasion, survival, and inflammation. In prostate cancer, an aberrant or persistent activation of the JAK/STAT signaling is related to tumor growth and disease progression, making this pathway an ideal therapeutic target. Here, we review the most recent literature on this topic, and we summarize the latest advances and future... (More)

The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway was originally identified as a key cellular mechanism mediating the action of cytokines, interferons, and growth factors for the control of gene expression. Extracellular signals mediated by cytokines are thus transduced through this pathway into transcriptional programs that regulate cell growth, differentiation, proliferation, invasion, survival, and inflammation. In prostate cancer, an aberrant or persistent activation of the JAK/STAT signaling is related to tumor growth and disease progression, making this pathway an ideal therapeutic target. Here, we review the most recent literature on this topic, and we summarize the latest advances and future challenges in therapeutically targeting the JAK/STAT pathway in prostate cancer.

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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Castration-resistant prostate cancer, Cytokines, IL-6, JAK/STAT pathway, Myeloid-derived suppressor cells, Prostate cancer, STAT3
in
Current Opinion in Endocrine and Metabolic Research
volume
10
pages
7 pages
publisher
Elsevier
external identifiers
  • scopus:85081744437
ISSN
2451-9650
DOI
10.1016/j.coemr.2020.02.004
language
English
LU publication?
yes
id
8872e90e-1185-4a90-9bc8-8bb682bef3cc
date added to LUP
2020-04-07 13:40:17
date last changed
2022-05-04 17:00:26
@article{8872e90e-1185-4a90-9bc8-8bb682bef3cc,
  abstract     = {{<p>The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway was originally identified as a key cellular mechanism mediating the action of cytokines, interferons, and growth factors for the control of gene expression. Extracellular signals mediated by cytokines are thus transduced through this pathway into transcriptional programs that regulate cell growth, differentiation, proliferation, invasion, survival, and inflammation. In prostate cancer, an aberrant or persistent activation of the JAK/STAT signaling is related to tumor growth and disease progression, making this pathway an ideal therapeutic target. Here, we review the most recent literature on this topic, and we summarize the latest advances and future challenges in therapeutically targeting the JAK/STAT pathway in prostate cancer.</p>}},
  author       = {{Canesin, Giacomo and Krzyzanowska, Agnieszka and Hellsten, Rebecka and Bjartell, Anders}},
  issn         = {{2451-9650}},
  keywords     = {{Castration-resistant prostate cancer; Cytokines; IL-6; JAK/STAT pathway; Myeloid-derived suppressor cells; Prostate cancer; STAT3}},
  language     = {{eng}},
  month        = {{02}},
  pages        = {{36--42}},
  publisher    = {{Elsevier}},
  series       = {{Current Opinion in Endocrine and Metabolic Research}},
  title        = {{Cytokines and Janus kinase/signal transducer and activator of transcription signaling in prostate cancer : overview and therapeutic opportunities}},
  url          = {{http://dx.doi.org/10.1016/j.coemr.2020.02.004}},
  doi          = {{10.1016/j.coemr.2020.02.004}},
  volume       = {{10}},
  year         = {{2020}},
}