ArticlePloS one2010
Role of STAT3 in in vitro transformation triggered by TRK oncogenes.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Nerve growth factor causes epinephrine release dysfunction by regulating phenotype alterations and the function of adrenal medullary chromaffin cells in mice with allergic rhinitis.Molecular medicine reports · 2023Article
- Article
- Selective inhibition of STAT3 signaling using monobodies targeting the coiled-coil and N-terminal domains.Nature communications · 2020Article
- Inhibition of protease-activated receptor-2 induces apoptosis in cervical cancer by inhibiting signal transducer and activator of transcription-3 signaling.The Journal of international medical research · 2019Article
- Neurotrophin Signaling and Stem Cells-Implications for Neurodegenerative Diseases and Stem Cell Therapy.Molecular neurobiology · 2017Review
- Neuroprotective Effect of Nanodiamond in Alzheimer's Disease Rat Model: a Pivotal Role for Modulating NF-κB and STAT3 Signaling.Molecular neurobiology · 2017Article
- Autocrine activity of BDNF induced by the STAT3 signaling pathway causes prolonged TrkB activation and promotes human non-small-cell lung cancer proliferation.Scientific reports · 2016Article
- TRKing down an old oncogene in a new era of targeted therapy.Cancer discovery · 2015Review
- Regulation of neurotrophin receptor (Trk) signaling: suppressor of cytokine signaling 2 (SOCS2) is a new player.Frontiers in molecular neuroscience · 2014Review
- Role of STAT3 in cancer metastasis and translational advances.BioMed research international · 2013Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TRK oncoproteins are chimeric versions of the NTRK1/NGF receptor and display constitutive tyrosine kinase activity leading to transformation of NIH3T3 cells and neuronal differentiation of PC12 cells. Signal Transducer and Activator of Transcription (STAT) 3 is activated in response to cytokines and growth factors and it has been recently identified as a novel signal transducer for TrkA, mediating the functions of NGF in nervous system. In this paper we have investigated STAT3 involvement in signalling induced by TRK oncogenes. We showed that TRK oncogenes trigger STAT3 phosphorylation both on Y705 and S727 residues and STAT3 transcriptional activity. MAPK pathway was involved in the induction of STAT3 phosphorylation. Interestingly, we have shown reduced STAT3 protein level in NIH3T3 transformed foci expressing TRK oncogenes. Overall, we have unveiled a dual role for STAT3 in TRK oncogenes-induced NIH3T3 transformation: i) decreased STAT3 protein levels, driven by TRK oncoproteins activity, are associated to morphological transformation; ii) residual STAT3 transcriptional activity is required for cell growth.
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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.