ArticleCell death & disease2026
The DAG/PKC/CREB1/TGF-β1 axis drives shear-wave elastography stiffness and malignant progression in triple-negative breast cancer via lipid metabolic reprogramming.
Article in Cell death & disease, 2026. 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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Who cites it
2 citing papers in PubMed.
- Nanomedicine targeting ECM stiffness: restoring mechanical homeostasis for cancer immunotherapy.Materials today. Bio · 2026Review
- Serum metabolic characteristics of interstitial lung disease: a potential link between endocrine aging and gut-derived metabolites.Frontiers in medicine · 2026Article
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Authors and funding
12 authors.
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Abstract
In clinical practice, triple-negative breast cancer (TNBC) patients with varying levels of lipid metabolism exhibit differences in tumor shear-wave elastography (SWE) stiffness and prognosis, but this association with unclear mechanism. In this study, a clinical cohort from FUSCC (n = 147) demonstrated that both elevated BMI and higher SWE stiffness were significantly associated with poorer long-term prognosis in TNBC patients, and these associations were further validated in multi-TNBC animal models. Our findings emphasize the role of SWE stiffness in capturing BMI-related alterations in the tumor mechanical microenvironment. Based on integrated lipidomic and transcriptomic analyses, we demonstrated that diacylglycerol (DAG) serves as a critical lipid molecule promoting elevated SWE stiffness and malignant progression. Mechanistically, DAG upregulates TGF-β1 expression through PKC-mediated enhancement of CREB1 phosphorylation in multiple TNBC cell lines, directly promoting TNBC progression and activating cancer-associated fibroblasts. This creates a self-sustaining feedback loop that accelerates malignancy. Finally, we confirmed that the DAG/PKC/CREB1/TGF-β1 signaling axis profoundly regulates SWE imaging stiffness in TNBC models, with further validation in clinical samples. Our study establishes SWE stiffness as a non-invasive imaging biomarker for the activation of this specific pro-metastatic pathway, providing a mechanistic basis for interpreting SWE features through a biological lens and paving the way for its application in prognosis prediction and tailored therapeutic strategies for high-risk TNBC patients.
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