ReviewMolecular biology reports2026
PI4K and PIPK families in breast cancer: subtype-specific oncogenic mechanisms and precision therapeutic strategies.
Review in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Breast cancer exhibits profound subtype heterogeneity, with luminal A/B, human epidermal growth factor receptor 2 (HER2)-positive, and triple-negative breast cancer (TNBC) showing distinct biological behaviours and therapeutic responses. Despite advances in targeted therapies, primary and acquired resistance remain a major clinical challenge. Phosphatidylinositol 4-kinases (PI4Ks) and phosphatidylinositol phosphate kinases (PIPKs) are key regulators of lipid signalling, metabolic reprogramming, cytoskeletal remodelling, and immune modulation-processes frequently dysregulated in breast cancer. This review summarizes their oncogenic mechanisms: luminal subtypes are frequently characterized by PI4KB amplification and PIP5K1A overexpression, promoting phosphatidylinositol 3-kinase-protein kinase B (PI3K-AKT) activation and endocrine resistance; HER2-positive subtypes are frequently associated with PI5P4Kβ co-amplification with ERBB2 and PI4KIIα-mediated HER2 signalling to enhance angiogenesis; TNBC is characterized by PIKfyve-mediated immune escape, PI4P5Kγ-driven glycolysis, and PI5P4Kα/β-regulated peroxisomal fatty acid β-oxidation (FAO). We discuss subtype-tailored therapies (small-molecule inhibitors, proteolysis-targeting chimeras (PROTACs), drug repurposing) and combination strategies, analyze resistance mechanisms (target compensation, metabolic adaptation), and propose overcoming strategies. Finally, we outline clinical translation via a multi-omics-guided precision matching model. This review provides insights into PI4K/PIPK roles in breast cancer progression and offers novel ideas for more effective precision therapies.
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