ArticleBreast cancer research : BCR2023
Key regulator PNPLA8 drives phospholipid reprogramming induced proliferation and migration in triple-negative breast cancer.
Article in Breast cancer research : BCR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Pathogenic variants of the mitochondrial copper chaperones SCO1 and SCO2 reshape their respective interactomes and disrupt cellular phospholipid metabolism.bioRxiv : the preprint server for biology · 2026Article
- Plasma acylcarnitine dysregulation associated with CPT1-mediated metabolism contributes to oral carcinogenesis.Scientific reports · 2026Article
- Stromal Laminin Subunit Alpha 3 is a Novel Prognostic Marker for Breast Cancer.Clinical Medicine Insights. Oncology · 2026Article
- Molecular cargo of small EVs from NSCLC patient BALF and plasma: unveiling their role in airway inflammation and immune regulation in a novel human 3D bronchial model.Cell communication and signaling : CCS · 2025Article
- Metabolomics as a tool for understanding and treating triple-negative breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Identifying potential biomarkers and molecular mechanisms related to arachidonic acid metabolism in vitiligo.Frontiers in molecular biosciences · 2025Article
- Plasma Metabolome Signatures to Predict Responsiveness to Neoadjuvant Chemotherapy in Breast Cancer.Cancers · 2024Article
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundTriple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype and leads to the poorest patient outcomes despite surgery and chemotherapy treatment. Exploring new molecular mechanisms of TNBC that could lead to the development of novel molecular targets are critically important for improving therapeutic options for treating TNBC.
methodsWe sought to identify novel therapeutic targets in TNBC by combining genomic and functional studies with lipidomic analysis, which included mechanistic studies to elucidate the pathways that tie lipid profile to critical cancer cell properties. Our studies were performed in a large panel of human breast cancer cell lines and patient samples.
resultsComprehensive lipid profiling revealed that phospholipid metabolism is reprogrammed in TNBC cells. We discovered that patatin-like phospholipase domain-containing lipase 8 (PNPLA8) is overexpressed in TNBC cell lines and tissues from breast cancer patients. Silencing of PNPLA8 disrupted phospholipid metabolic reprogramming in TNBC, particularly affecting the levels of phosphatidylglycerol (PG), phosphatidylcholine (PC), lysophosphatidylcholine (LPC) and glycerophosphocholine (GPC). We showed that PNPLA8 is essential in regulating cell viability, migration and antioxidation in TNBC cells and promoted arachidonic acid and eicosanoid production, which in turn activated PI3K/Akt/Gsk3β and MAPK signaling.
conclusionsOur study highlights PNPLA8 as key regulator of phospholipid metabolic reprogramming and malignant phenotypes in TNBC, which could be further developed as a novel molecular treatment target.
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