ArticleBiochemistry and biophysics reports2020
Neuroplastinβ-mediated upregulation of solute carrier family 22 member 18 antisense (SLC22A18AS) plays a crucial role in the epithelial-mesenchymal transition, leading to lung cancer cells' enhanced motility.
Article in Biochemistry and biophysics reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 6 citations in OpenAlex.
- Identification of a novel signature in progression of non-small cell lung cancer based on HdWGCNA and in vitro validation.BMC medical genomics · 2026Article
- Enhanced design of pCMViR-TSC plasmid vector for sustainably high cargo gene expression in mammalian cells.In vitro cellular & developmental biology. Animal · 2024Article
- The functions and regulatory pathways of S100A8/A9 and its receptors in cancers.Frontiers in pharmacology · 2023Review
- Neuroplastin in Neuropsychiatric Diseases.Genes · 2021Review
- The Roles of ImprintedCancers · 2020Article
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Authors and funding
14 authors at 5 institutions in 4 countries.
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Abstract
Our recent study revealed an important role of the neuroplastin (NPTN)β downstream signal in lung cancer dissemination in the lung. The molecular mechanism of the signal pathway downstream of NPTNβ is a serial activation of the key molecules we identified: tumor necrosis factor (TNF) receptor-associated factor 2 (TRAF2) adaptor, nuclear factor (NF)IA/NFIB heterodimer transcription factor, and SAM pointed-domain containing ETS transcription factor (SPDEF). The question of how dissemination is controlled by SPDEF under the activated NPTNβ has not been answered. Here, we show that the NPTNβ-SPDEF-mediated induction of solute carrier family 22 member 18 antisense (SLC22A18AS) is definitely required for the epithelial-mesenchymal transition (EMT) through the NPTNβ pathway in lung cancer cells.
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