ArticleOncoscience2019
Suppression of vascular endothelial growth factor expression in breast cancer cells by microRNA-125b-mediated attenuation of serum amyloid A activating factor-1 level.
Article in Oncoscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Angioregulatory microRNAs in breast cancerJournal of advanced research · 2022Review
- Essential functions of miR-125b in cancer.Cell proliferation · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased level of an inflammation-responsive transcription factor called serum amyloid A-activating factor (SAF-1) has been linked to the pathogenesis in human breast cancer. SAF-1 is found to promote vascular endothelial growth factor (VEGF) expression in breast carcinoma cells and boost angiogenesis. In an effort to develop a cellular mechanism to control VEGF expression, we sought to limit SAF-1 activity in breast cancer cells. We report here several targets within the SAF-1 mRNA for binding of microRNA-125b (miR-125b) and we show that VEGF expression is reduced in breast cancer cells when SAF-1 level is reduced with the microRNA action. Within the 3' un-translated region (UTR) of SAF-1 transcript, we have identified four highly conserved miR-125b responsive elements. We show that these miR-125b binding sites mediate repression of SAF-1 by miR-125b. Ectopic expression of miR-125b in nonmetastatic and metastatic breast cancer cells repressed SAF-1-mediated activity on VEGF promoter function and inhibited cancer cell migration and invasion potentials
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