Stat3 inhibits WTX expression through up‐regulation of microRNA‐370 in Wilms tumor
Abstract
Wilms tumor (WT) is a genetically heterogeneous childhood kidney tumor. Several genetic mutations have been identified in WT patients, including inactivation of WTX, somatic stabilizing CTNNB1, and p53 mutations. However, the molecular mechanisms in tumorigenesis remain largely unexplored. Stat3 is a transcription factor that can promote oncogenesis. Stat3 activation is commonly viewed as crucial for multiple tumor proliferation and metastasis. We show that Stat3 is highly activated in Wilms tumor tissues compared to those in adjacent tissues. IL-6 treatment or transfection of a constitutively activated Stat3 in G401 cells promotes cell proliferation. At the molecular level, we further elucidate that Stat3 inhibits WTX expression through up-regulation of microRNA-370. Our results suggest that Stat3/miR-370/WTX regulatory axis might be a critical mechanism in Wilms tumor cells.
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STAT3 is persistently active in Wilms' tumor, where it transcriptionally upregulates the microRNA miR-370, which in turn regulates cell proliferation and tumorigenicity in mice.
“For example, STAT3 is persistently active in Wilms’ tumor, a genetically heterogeneous childhood kidney cancer, where it transcriptionally upregulates the microRNA miR-370, which in turn regulates cell proliferation and tumorigenicity in mice.76”
From Critical analysis of the potential for targeting STAT3 in human malignancy (2013) · cites this paper as [76]
Cites
Novel roles of unphosphorylated STAT3 in oncogenesis and transcriptional regulation
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Activation of STAT3 is a marker of poor prognosis in human colorectal cancer
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Critical analysis of the potential for targeting STAT3 in human malignancy
Grandis, J., & Peyser (2013) · OncoTargets and Therapy · doi:10.2147/ott.s47903 · Cited by 24 · see citing works
“These cells also exhibit downregulation of the proteins p21 and p27 (which inhibit progress through the cell cycle) and upregulation of cyclin D1, illustrating novel mechanisms downstream of STAT3 that contribute to its proliferative capacity.(76)”
Influential
- Authors
- Cao, X., Liu, D., Yan, X., Zhang, Y., Yuan, L., Zhang, T., Fu, M., Zhou, Y., & Wang, J.
- Affiliations
- Soochow University (CN)
- Shanghai Jiao Tong University (CN)
- Corresponding author
- Wang, Jian
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2013-01-17
- Volume
- 587
- Issue
- 6
- Pages
- 639-644
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W2006519367
- Cited by
- 41
- References
- 3
- Citations by year
- 2025: 1 · 2023: 3 · 2022: 1 · 2021: 2 · 2020: 6 · 2019: 5 · 2018: 1 · 2017: 4 · 2016: 8 · 2015: 5 · 2014: 2 · 2013: 3
- FWCI
- 2.69
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- FEBS Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Natural Science Foundation of Jiangsu Province of China (BK2011312)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Renal and related cancers
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Keywords
- STAT3, WTX, Wilms tumor, transcriptional repression, IL-6 signaling, cell proliferation, tumor suppressor regulation
- MeSH terms
- Humans, Luciferases, Wilms Tumor, Plasmids, Transcription, Genetic, Transfection, Signal Transduction, Interleukin-6, Gene Expression Regulation, Neoplastic, Genes, Reporter, Tumor Suppressor Proteins, RNA, Small Interfering, MicroRNAs, Adaptor Proteins, Signal Transducing, Cell Proliferation, Green Fluorescent Proteins, STAT3 Transcription Factor, Tumor Microenvironment, Primary Cell Culture
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