The DOI matches its Crossref record; 53 of the 64 references it cites were found in a registry or an index.
Constitutively Active Stat3 Enhances Neu-Mediated Migration and Metastasis in Mammary Tumors via Upregulation of Cten
Open accessPublished version of a preprint
Abstract
The transcription factor signal transducer and activator of transcription 3 (STAT3) is constitutively activated in tumors of different origin, but the molecular bases for STAT3 requirement are only partly understood. To evaluate the contribution of enhanced Stat3 activation in a controlled model system, we generated knock-in mice wherein a mutant constitutively active Stat3C allele replaces the endogenous wild-type allele. Stat3C could enhance the tumorigenic power of the rat Neu oncogene in mouse mammary tumor virus (MMTV)-Neu transgenic mice, triggering the production of earlier onset, more invasive mammary tumors. Tumor-derived cell lines displayed higher migration, invasion, and metastatic ability and showed disrupted distribution of cell-cell junction markers mediated by Stat3-dependent overexpression of the COOH terminal tensin-like (Cten) focal adhesion protein, which was also significantly upregulated in Stat3C mammary tumors. Importantly, the proinflammatory cytokine interleukin-6 could mediate Cten induction in MCF10 cells in an exquisitely Stat3-dependent way, showing that Cten upregulation is a feature of inflammation-activated Stat3. In light of the emerging pivotal role of Stat3 in connecting inflammation and cancer, our identification of Cten as a Stat3-dependent mediator of migration provides important new insights into the oncogenic role of Stat3, particularly in the breast.
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“The IL-6–STAT3 pathway is involved in the epithelial–mesenchymal transition (EMT) (131, 132), tumor migration (133), cancer stemness (130, 134, 135) and the induction of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF), two key players for angiogenesis (136–140).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [133]
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Background
Research works printed but not linked: 4
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Cited by
Sorted by citations
IL-6 in inflammation, autoimmunity and cancer
Hirano, T. (2021) · International Immunology · doi:10.1093/intimm/dxaa078 · Cited by 1,453
“The IL-6–STAT3 pathway is involved in the epithelial–mesenchymal transition (EMT) (131, 132), tumor migration (133), cancer stemness (130, 134, 135) and the induction of hypoxia-inducible factor-1 α (HIF-1 α ) and vascular endothelial growth factor (VEGF), two key players for angiogenesis (136–140).”
BackgroundLaklai, H., Miroshnikova, Y. A., Pickup, M. W., Collisson, E. A., Kim, G., Barrett, A., Hill, R. C., Lakins, J. N., Schlaepfer, D. D., Mouw, J. K., et al. (2016) · Nature Medicine · doi:10.1038/nm.4082 · Cited by 614
Self-citationTherapeutically exploiting STAT3 activity in cancer — using tissue repair as a road map
Huynh, J., Chand, A. L., Gough, D. J., & Ernst, M. (2018) · Nature reviews. Cancer · doi:10.1038/s41568-018-0090-8 · Cited by 522
The role of intratumoral and systemic IL-6 in breast cancer
Dethlefsen, C., Højfeldt, G. W., & Højman, P. (2013) · Breast Cancer Research and Treatment · doi:10.1007/s10549-013-2488-z · Cited by 372
Masjedi, A., Hashemi, V., Hojjat-Farsangi, M., Ghalamfarsa, G., Azizi, G., Yousefi, M., & Jadidi-Niaragh, F. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.09.177 · Cited by 303
Metadata
- Authors
- Barbieri, I., Pensa, S., Pannellini, T., Quaglino, E., Maritano, D., Demaria, M., Voster, A., Turkson, J., Cavallo, F., Watson, C. J., Provero, P., Musiani, P., & Poli, V.
- Affiliations
- University of Central Florida (US)
- ORCID
- Venue
- Cancer Research
- Published
- 2010-03-14
- Volume
- 70
- Issue
- 6
- Pages
- 2558-2567
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2004465485
- Cited by
- 148
- References
- 64
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 3 · 2023: 12 · 2022: 6 · 2021: 4 · 2020: 10 · 2019: 6 · 2018: 12 · 2017: 7 · 2016: 10 · 2015: 9 · 2014: 17 · 2013: 11 · 2012: 16
- FWCI
- 6.95
- Type
- journal article
- Language
- en
- Open access
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion)
- Journal of International Crisis and Risk Communication Research (submittedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- Funders
- Fondazione CRT
- Ministero dell'Università e della Ricerca
- National Cancer Institute (R01CA128865)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- STAT3, CTEN, mammary tumors, breast cancer, tumor cell migration, tumor invasion, metastasis, neu oncogene, mouse mammary tumor virus, cell-cell contact, interleukin-6, inflammation and cancer, oncogenic signaling
- MeSH terms
- Tensins, Animals, Breast Neoplasms, Cell Movement, Cell Nucleus, Female, Humans, Lung Neoplasms, Male, Mammary Neoplasms, Experimental, Mice, Transgenic, Microfilament Proteins, Phosphorylation, Transcription, Genetic, Up-Regulation, Erb-b2 Receptor Tyrosine Kinases, Cell Line, Tumor, STAT3 Transcription Factor, Mice
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