ArticleOncogene2004
STAT3 and MITF cooperatively induce cellular transformation through upregulation of c-fos expression.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- Dual-specificity tyrosine-regulated kinase 4 modulates the STAT3-FOS signaling axis to inhibit hepatitis B virus replicationInternational journal of biological sciences · 2025Article
- Joint Genomic and Transcriptomic Analysis Reveals Candidate Genes Associated with Plumage Color Traits in Matahu Ducks.Animals : an open access journal from MDPI · 2024Article
- Current progress and prospects for G protein-coupled estrogen receptor in triple-negative breast cancer.Frontiers in cell and developmental biology · 2024Review
- Retinal pigment epithelium transcriptome analysis in chronic smoking reveals a suppressed innate immune response and activation of differentiation pathways.Free radical biology & medicine · 2020Article
- Focal adhesion kinase (FAK) activation by estrogens involves GPER in triple-negative breast cancer cells.Journal of experimental & clinical cancer research : CR · 2019Article
- Article
- HPV16E6-dependent c-fos expression contributes to AP-1 complex formation in SiHa cells.Mediators of inflammation · 2011Article
- Article
- MiTF links Erk1/2 kinase and p21 CIP1/WAF1 activation after UVC radiation in normal human melanocytes and melanoma cells.Molecular cancer · 2010Article
- NF-kappaB/STAT3/PI3K signaling crosstalk in iMyc E mu B lymphoma.Molecular cancer · 2010Article
- Article
- Heregulin-beta promotes matrix metalloproteinase-7 expression via HER2-mediated AP-1 activation in MCF-7 cells.Molecular and cellular biochemistry · 2008Article
- Article
- STAT3 inhibition in prostate and pancreatic cancer lines by STAT3 binding sequence oligonucleotides: differential activity between 5' and 3' ends.Molecular cancer therapeutics · 2008Article
- STAT6 Inhibits TGF-beta1-mediated Foxp3 induction through direct binding to the Foxp3 promoter, which is reverted by retinoic acid receptor.The Journal of biological chemistry · 2008Article
- Unphosphorylated STAT3 accumulates in response to IL-6 and activates transcription by binding to NFkappaB.Genes & development · 2007Article
- Analysis of KRAP expression and localization, and genes regulated by KRAP in a human colon cancer cell line.Journal of human genetics · 2007Article
- Signal transduction of inflammatory cytokines and tumor development.Cancer science · 2006Review
- Loss of SOCS3 in T helper cells resulted in reduced immune responses and hyperproduction of interleukin 10 and transforming growth factor-beta 1.The Journal of experimental medicine · 2006Article
- T-cell growth transformation by herpesvirus saimiri is independent of STAT3 activation.Journal of virology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The signal transducer and activator of transcription (STAT) family proteins are transcription factors critical in mediating cytokine signaling. Among them, STAT3 is frequently activated in a number of human cancers and transformed cell lines and is implicated in tumorigenesis. However, although constitutively activated STAT3 mutant (STAT3C) leads to cellular transformation, its transformation potential such as colony-forming activity in soft-agar is much weaker than that of v-src. To identify tumorigenic factors that cooperatively induce cellular transformation with STAT3C, we screened the retroviral cDNA library. We found that the microphthalmia-associated transcription factor (MITF), an essential transcription factor for melanocyte development and pigmentation, induces anchorage-independent growth of NIH-3T3 cells in cooperation with STAT3C. Microarray analysis revealed that c-fos is highly expressed in transformants expressing STAT3C and MITF. Promoter analysis and chromatin immunoprecipitation assay suggested that both STAT3 and MITF can cooperatively upregulate the c-fos gene. In addition, the transformation of NIH-3T3 cells by both MITF and STAT3C was significantly suppressed by a dominant-negative AP-1 retrovirus. These data indicate that MITF and STAT3 cooperatively induce c-fos, resulting in cellular transformation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.