ArticleAnnals of biomedical engineering2025
Chemotherapy-Induced Cell-Surface GRP78 Expression as a Prognostic Marker for Invasiveness of Metastatic Triple-Negative Breast Cancer.
Article in Annals of biomedical engineering, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- GRP78 dysregulation: A proposed molecular mechanism linking the tumor microenvironment to sepsis susceptibility in patients with cancer (Review).International journal of molecular medicine · 2026Review
- Cell surface GRP78 and the UPR pathway as novel promising therapeutic targets in cancer: an insight into the treatment of acute leukemia by using GRP78-CART cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Bioactive Profiling and Evaluation of Anti-Proliferative Potential ofLife (Basel, Switzerland) · 2026Article
- A Curcumin-Derived HSP70 Inhibitor Disrupts Lysosomal Function to Suppress Triple-Negative Breast Cancer Progression.Cell proliferation · 2026Article
- Computational characterization of GRP78 binding sites on mitochondrial GPX4: implications for targeting ferroptosis in triple-negative breast cancer.Scientific reports · 2026Article
- Targeted Degradation of sGRP78 Alleviates the Immunosuppressive Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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4 authors.
Funding
Abstract
Metastasis remains the leading cause (90%) of cancer-related mortality, especially in metastatic triple-negative breast cancer (TNBC). Improved understanding of molecular drivers in the metastatic cascade is crucial, to find accurate prognostic markers for invasiveness after chemotherapy treatment. Current breast cancer chemotherapy treatments include doxorubicin and paclitaxel, inducing various effects, such as the unfolded protein response (UPR). The key regulator of the UPR is the 78-kDa glucose-regulated protein (GRP78), which is associated with metastatic disease, although, its expression level in the context of invasiveness is still controversial. We evaluate doxorubicin effects on TNBC cells, identifying GRP78 subpopulations linked to invasiveness. Specifically, we evaluate the motility and invasiveness of GRP78 positive vs. negative cell subpopulations by two different assays: the in vitro Boyden chamber migration assay and our innovative, rapid (2-3 h) clinically relevant, mechanobiology-based invasiveness assay. We validate chemotherapy-induced increase in the subpopulation of cell-surface GRP78(+) in two human, metastatic TNBC cell lines: MDA-MB-231 and MDA-MB-468. The GRP78(+) cell subpopulation exhibits reduced invasiveness and metastatic potential, as compared to whole-population control and to the GRP78(-) cell subpopulation, which are both highly invasive. Thus, using our innovative, clinically relevant assay, we rapidly (on clinical timescale) validate that GRP78(-) cells are likely linked with invasiveness, yet also demonstrate that combination of the GRP78(+) and GRP78(-) cells could increase the overall metastatic potential. Our results and approach could provide patient-personalized predictive marker for the expected benefits of chemotherapy in TNBC patients and potentially reveal non-responders to chemotherapy while also allowing evaluation of the clinical risk for metastasis.
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