ArticleOpen medicine (Warsaw, Poland)2022
EphA3 targeted by miR-3666 contributes to melanoma malignancy via activating ERK1/2 and p38 MAPK pathways.
Article in Open medicine (Warsaw, Poland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Targeting the Golgi apparatus enhances PD-L1 blockade and synergizes with oxaliplatin to improve immunotherapy efficacy.The Journal of biological chemistry · 2026Article
- Eph/ephrin-mediated immune modulation: a potential therapeutic target.Frontiers in immunology · 2025Review
- BS148 Reduces the Aggressiveness of Metastatic Melanoma via Sigma-2 Receptor Targeting.International journal of molecular sciences · 2023Article
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
Melanoma is a rare, fatal type of skin tumor. Although EPH receptor A3 (EphA3) is deregulated in melanoma, its detailed role remained uncharacterized. Using real time quantitative PCR analysis and western blotting, EphA3 was identified to be upregulated in melanoma tissues and cells, while miR-3666 showed an opposite expression trend. Cell counting kit-8, scratch wound, and
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Registered trials
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