Next Article in Journal
The Targeting of RNA Polymerase I Transcription Using CX-5461 in Combination with Radiation Enhances Tumour Cell Killing Effects in Human Solid Cancers
Next Article in Special Issue
STAT3 and STAT5 Targeting for Simultaneous Management of Melanoma and Autoimmune Diseases
Previous Article in Journal
FOXO1 Confers Maintenance of the Dark Zone Proliferation and Survival Program and Can Be Pharmacologically Targeted in Burkitt Lymphoma
Previous Article in Special Issue
Hepatic Stress Response in HCV Infection Promotes STAT3-Mediated Inhibition of HNF4A-miR-122 Feedback Loop in Liver Fibrosis and Cancer Progression

STAT3 and STAT5 Activation in Solid Cancers

Department of Biochemistry and Molecular Medicine, Université de Montréal, C.P. 6128, Succ. Centre-Ville, Montréal, QC, H3C 3J7, Canada
CRCHUM, 900 Saint-Denis St, Montréal, QC H2X 0A9, Canada
Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna 1210, Austria
Author to whom correspondence should be addressed.
Cancers 2019, 11(10), 1428;
Received: 1 August 2019 / Revised: 14 September 2019 / Accepted: 18 September 2019 / Published: 25 September 2019
(This article belongs to the Special Issue Targeting STAT3 and STAT5 in Cancer)
The Signal Transducer and Activator of Transcription (STAT)3 and 5 proteins are activated by many cytokine receptors to regulate specific gene expression and mitochondrial functions. Their role in cancer is largely context-dependent as they can both act as oncogenes and tumor suppressors. We review here the role of STAT3/5 activation in solid cancers and summarize their association with survival in cancer patients. The molecular mechanisms that underpin the oncogenic activity of STAT3/5 signaling include the regulation of genes that control cell cycle and cell death. However, recent advances also highlight the critical role of STAT3/5 target genes mediating inflammation and stemness. In addition, STAT3 mitochondrial functions are required for transformation. On the other hand, several tumor suppressor pathways act on or are activated by STAT3/5 signaling, including tyrosine phosphatases, the sumo ligase Protein Inhibitor of Activated STAT3 (PIAS3), the E3 ubiquitin ligase TATA Element Modulatory Factor/Androgen Receptor-Coactivator of 160 kDa (TMF/ARA160), the miRNAs miR-124 and miR-1181, the Protein of alternative reading frame 19 (p19ARF)/p53 pathway and the Suppressor of Cytokine Signaling 1 and 3 (SOCS1/3) proteins. Cancer mutations and epigenetic alterations may alter the balance between pro-oncogenic and tumor suppressor activities associated with STAT3/5 signaling, explaining their context-dependent association with tumor progression both in human cancers and animal models. View Full-Text
Keywords: solid cancers; cell cycle; apoptosis; inflammation; mitochondria; stemness; tumor suppression solid cancers; cell cycle; apoptosis; inflammation; mitochondria; stemness; tumor suppression
Show Figures

Figure 1

MDPI and ACS Style

Igelmann, S.; Neubauer, H.A.; Ferbeyre, G. STAT3 and STAT5 Activation in Solid Cancers. Cancers 2019, 11, 1428.

AMA Style

Igelmann S, Neubauer HA, Ferbeyre G. STAT3 and STAT5 Activation in Solid Cancers. Cancers. 2019; 11(10):1428.

Chicago/Turabian Style

Igelmann, Sebastian, Heidi A. Neubauer, and Gerardo Ferbeyre. 2019. "STAT3 and STAT5 Activation in Solid Cancers" Cancers 11, no. 10: 1428.

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Back to TopTop