ArticleClinical & experimental metastasis2003
Overexpression of autocrine motility factor receptor (AMFR) in NIH3T3 fibroblasts induces cell transformation.
Article in Clinical & experimental metastasis, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 22 citations in OpenAlex.
- Betulinic Acid Exerts Cytotoxic Activity Against Multidrug-Resistant Tumor Cells via Targeting Autocrine Motility Factor Receptor (AMFR).Frontiers in pharmacology · 2018Article
- Gp78 E3 Ubiquitin Ligase: Essential Functions and Contributions in Proteostasis.Frontiers in cellular neuroscience · 2017Review
- gp78 is specifically expressed in human prostate cancer rather than normal prostate tissue.Journal of molecular histology · 2013Article
- The Unfolded Protein Response, Degradation from Endoplasmic Reticulum and Cancer.Genes & cancer · 2010Article
- Article
- Identification of novel pro-migratory, cancer-associated genes using quantitative, microscopy-based screening.PloS one · 2008Article
- Ubiquitin ligases, critical mediators of endoplasmic reticulum-associated degradation.Seminars in cell & developmental biology · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Autocrine motility factor receptor (AMFR) is a cell surface glycoprotein of 78000 molecular weight (gp78), regulating cell motility signaling in vitro and metastasis in vivo. To test whether AMFR could be a common mediator of transformation and oncogenic itself, we transfected NIH3T3 fibroblast cells with expression vectors carrying the full-length cDNA for mouse AMFR and evaluated the effects of increased AMFR on transforming potential. The cells stably expressing high levels of AMFR as a result of transfection displayed a complete morphological change and acquired the ability to grow even in low serum. Furthermore, they were anchorage-independent for growth in soft agar and more motile in phagokinetic track assay. Interestingly, the enhanced expression of AMFR produced tumors in nude mice. Our findings provide a direct evidence that overexpression of the AMFR is associated with the acquisition of a transformation phenotype.
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What OpenQuestion holds
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.