# CGF-Conditioned Medium Modulates Astrocytic Differentiation and Invasiveness in U87MG Glioblastoma Cells

**Authors:** Laura Giannotti, Benedetta Di Chiara Stanca, Francesco Spedicato, Christian Demitri, Eleonora Stanca, Andrea Palermo, Franco Ferrante, Fabrizio Damiano, Maria Antonietta De Sangro, Luciano Abbruzzese, Luisa Siculella

PMC · DOI: 10.3390/biology14101461 · Biology · 2025-10-21

## TL;DR

This study shows that blood-derived growth factors can reduce the aggressiveness of glioblastoma cells, making them more like normal brain cells.

## Contribution

The study demonstrates that CGF-conditioned medium can modulate glioblastoma cell behavior toward a less aggressive, astrocytic phenotype.

## Key findings

- CGF-CM initially increased cell viability but later reduced proliferation and migration.
- Treated cells showed astrocyte-like features and increased expression of GFAP.
- GBM-associated markers like AQP-4 and S100B were downregulated with CGF-CM treatment.

## Abstract

Glioblastoma is one of the most aggressive brain tumors, known for its ability to change shape and behavior, which makes it very difficult to treat. In our study, we tested whether substances naturally present in blood, called growth factors, could influence the behavior of glioblastoma cells grown in the laboratory. To do this, we used a special preparation, obtained from whole venous blood, rich in these growth factors, and exposed tumor cells to it for over one week. In the first days, the treated cells appeared more active, but later their ability to multiply and move decreased. Morphologically, the tumor cells began to show features more similar to normal brain support cells, called astrocytes, which are less harmful than tumor cells. We also observed that proteins typically linked to tumor aggressiveness decreased, while proteins typical of normal brain cells increased. These findings suggest that natural blood-derived preparations may encourage glioblastoma cells to adopt a less aggressive state. This knowledge may help future research explore new, more natural strategies to reduce tumor aggressiveness and possibly improve therapeutic approaches for this devastating disease.

Background: Glioblastoma (GBM) is a highly aggressive tumor characterized by elevated plasticity and poor differentiation. Platelet-derived preparations such as Concentrated Growth Factors (CGF) are rich in bioactive molecules, but their effects on tumor biology remain underexplored. Methods: U87MG glioblastoma cells were cultured with a conditioned medium obtained from CGF over 14 days (CGF-CM). We analyzed cell viability, morphology, DNA integrity, migration, proliferation, and expression of astrocytic markers. Results: CGF-CM treatment induced early enhancement of cell viability, followed by decreased proliferation and reduced migration at later time points. Morphological analyses revealed astrocyte-like features. The expression of glial fibrillary acidic protein (GFAP), an astrocytic marker, and its α/δ isoform ratio increased over time, while GBM -GBM-associated markers, such as AQP-4 and S100B, were downregulated. Conclusions: Our findings demonstrate that CGF-CM modulates the phenotypic plasticity of U87MG cells and promotes differentiation toward an astroglial-like profile. These results provide a basis for future studies on the modulation of GBM aggressiveness using bioactive autologous derivatives.

## Linked entities

- **Proteins:** GFAP (glial fibrillary acidic protein), AQP4 (aquaporin 4), S100B (S100 calcium binding protein B)
- **Diseases:** Glioblastoma (MONDO:0018177), GBM (MONDO:0018177)

## Full-text entities

- **Genes:** GFAP (glial fibrillary acidic protein) [NCBI Gene 2670] {aka ALXDRD}, S100B (S100 calcium binding protein B) [NCBI Gene 6285] {aka NEF, S100, S100-B, S100beta}, AQP4 (aquaporin 4) [NCBI Gene 361] {aka MIWC, MLC4, WCH4, hAQP4}
- **Diseases:** tumor (MESH:D009369), GBM (MESH:D005909)
- **Chemicals:** CGF (-)
- **Cell lines:** U87MG — Homo sapiens (Human), Glioblastoma, Cancer cell line (CVCL_0022)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12561328/full.md

## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12561328/full.md

## References

45 references — full list in the complete paper: https://tomesphere.com/paper/PMC12561328/full.md

---
Source: https://tomesphere.com/paper/PMC12561328