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Cancer Technologies

Cancer Technologies - Poster Session C & D

V35 - SDF-1 induced mesenchymal transition enhances confined migration in GBM

Friday, October 10, 2025
10:00 AM - 11:00 AM PDT
Location: Exhibit Hall F, G & H

Introduction: : Glioblastoma (GBM) is an aggressive primary brain tumor originating in glial cells, marked by rapid growth and invasion into healthy brain tissue. Current treatments are insufficient, underscoring the need to uncover mechanisms driving its progression. Many GBM tumors exhibit tropism toward the subventricular zone (SVZ), infiltrating through dense parenchyma to localize within this neurogenic niche—a hallmark associated with worsened overall survival (Figure 1). The SVZ, a reservoir for neural stem cells, secretes stromal cell-derived factor 1 (SDF-1) to maintain its niche. SDF-1 has been implicated in malignancy and invasion across various cancers and may contribute to GBM’s confined migration toward the SVZ.
Beyond chemotaxis, SDF-1 engages intracellular signaling via its receptor CXCR4, altering tumor phenotype. In other cancers, SDF-1/CXCR4 activation of NF-κB induces epithelial-to-mesenchymal transition (EMT) and a cancer stem cell (CSC)-like state. For instance, SDF-1 overexpression in carcinoma cells activates NF-κB, upregulates mesenchymal markers such as ZEB1 and Vimentin, and increases stem factors like SOX2. We hypothesize that similar signaling in GBM promotes EMT and stemness—linking chemotactic tropism to invasive, therapy-resistant phenotypes.
Understanding SDF-1’s role in GBM infiltration may reveal new therapeutic targets. In this study, we leveraged bioengineering platforms and molecular tools to evaluate how SDF-1 regulates GBM phenotype and confined migration. Our goal was to investigate the impact of SDF-1 stimulation on GBM phenotype and invasion potential using both molecular assays and novel bioengineering approaches.

Materials and

Methods: : U87-MG GBM cells were cultured in standard DMEM media and treated with 100 ng/ml SDF-1. Western blotting assessed protein expression, including ZEB1, a key mesenchymal marker, and migration was evaluated using transwell assays with SDF-1 gradients and bioengineered microchannels mimicking confined spaces. Cells were imaged and analyzed using ImageJ. Prism10 was used to statistically analyze and produce graphs.

Results, Conclusions, and Discussions:: SDF-1 exposure significantly increased ZEB1 expression over 3 days, indicating proneural-to-mesenchymal transition (PMT) induction (Figure 2). Migration assays demonstrated enhanced motility and invasion in SDF-1-treated cells compared to controls. Under confinement, SDF-1-treated cells maintained faster migration through 5 µm and 20 µm channels, suggesting improved invasive potential in brain tissue (Figure 3). These findings identify SDF-1 as a promoter of PMT and invasion, crucial drivers of GBM progression. Targeting SDF-1 may reduce tumor aggressiveness, offering a new therapeutic avenue. Further investigation into the molecular pathways underlying these effects could yield transformative treatments for GBM.

Acknowledgements and/or References (Optional): :