ArticleOpen life sciences2025
ABI3BP can inhibit the proliferation, invasion, and epithelial-mesenchymal transition of non-small-cell lung cancer cells.
Article in Open life sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Comparative omics reveals conserved extracellular matrix signatures during mammary tumor progression.Frontiers in oncology · 2026Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer, especially non-small-cell lung cancer (NSCLC), has a poor 5-year survival rate below 20%, with factors like smoking, air pollution, and genetic mutations contributing to its development. ABI3BP, an extracellular matrix protein, inhibits NSCLC progression by regulating key signaling pathways; however, its exact mechanisms remain elusive. This study aimed to explore ABI3BP's role in NSCLC and its impact on these pathways. We found that ABI3BP expression was significantly reduced in NSCLC cells compared to normal controls. Overexpression of ABI3BP in NSCLC cells resulted in a substantial reduction in cell growth and motility and induced cell cycle arrest. Furthermore, its overexpression suppressed the epithelial-mesenchymal transition (EMT) process in NSCLC cells. In addition, ABI3BP overexpression inhibited the MAPK/ERK pathway in NSCLC cells. Collectively, ABI3BP functions as a tumor suppressor in NSCLC by targeting the MAPK/ERK axis, thereby regulating cell proliferation, motility, and EMT. These findings suggest that ABI3BP represents a potential therapeutic target for NSCLC treatment.
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