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Type of publication: Journal Article
Type of document: Full Paper

Year: 2015

Authors: Pencik, J; Wiebringhaus, R; Susani, M; Culig, Z; Kenner, L

Title: IL-6/STAT3/ARF: the guardians of senescence, cancer progression and metastasis in prostate cancer.

Source: Swiss Med Wkly. 2015; 145:w14215

Authors Vetmeduni Vienna:

Kenner Lukas

Vetmed Research Units
Institute of Pathology, Pathology of Laboratory Animals

Prostate cancer is one of the most prevalent forms of cancer in men worldwide. It remains a clinical challenge to identify lethal metastatic prostate cancers, which escape standard therapeutic intervention. Aberrant interleukin-6 (IL-6) / signal transducer and activator of transcription-3 (STAT3) signalling and loss of p53 occur during prostate cancer progression to metastatic disease. The abnormality of the IL-6/STAT3/p53 axis is frequently accompanied by other genetic alterations; however, its potential role as an important mediator of oncogenic reprogramming, invasion and metastatic transformation remains unknown. The failure of anti-IL-6 treatments is still unexplained and may be due to an incomplete understanding of the mechanism of the in vivo role of IL-6/STAT3 in prostate cancer. The identification of the alternative reading frame protein (ARF) / murine double minute protein (MDM2) / p53 tumour suppressor pathway potentially involving the IL-6/STAT3 axis as a restricting factor in prostate cancer deficient in the tumour suppressor phosphatase and tensin homologue (PTEN) opened new avenues to currently available therapies. This review summarises the current knowledge on the role of crucial pathways driving prostate cancer progression as well as metastatic disease and discusses the potential use of novel specific target molecules and how it can be exploited to avoid overtreatment and increase quality of life.

Keywords Pubmed: Animals
Disease Models, Animal
Disease Progression
Neoplasm Metastasis
PTEN Phosphohydrolase/genetics*
Prostatic Neoplasms/genetics*
Prostatic Neoplasms/therapy
Quality of Life
STAT3 Transcription Factor/genetics*
Signal Transduction*
Tumor Suppressor Protein p53/genetics*

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