ArticleScientific reports2025
BNIP3 is a key driver of breast cancer progression and a novel glycolysis-regulating biomarker.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Unfolded Protein Response Pathways in Cancer: Mechanisms, Tumor Biology and Therapeutic Opportunities.Molecular diagnosis & therapy · 2026Review
- Mitochondrial Quality Control in Age-Related Diseases: From Molecular Architecture to Precision Therapeutics.Antioxidants (Basel, Switzerland) · 2026Review
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6 authors.
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Abstract
Breast cancer (BC) represents a leading cause of cancer-related mortality among women, with glycolysis and immunomodulation playing pivotal roles in its progression. This study, by integrating bioinformatics analyses and in vitro and in vivo experiments, elucidates the mechanism of action of the mitochondrial protein BNIP3 in BC. The results demonstrate that BNIP3 is aberrantly overexpressed in BC tissues and cell lines, and is significantly associated with poor prognosis. Silencing BNIP3 can suppress glycolysis in vitro and in vivo (by reducing lactate production and glucose uptake) and inhibit tumor growth. Immune infiltration analysis reveals that high BNIP3 expression induces an immunosuppressive microenvironment, characterized by a reduction in CD8
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