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Microglia and glioblastoma heterocellular interplay sustains tumour growth and proliferation as an off‐target effect of radiotherapy.
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- المؤلفون: Alberghina, Cristiana; Torrisi, Filippo; D'Aprile, Simona; Longhitano, Lucia; Giallongo, Sebastiano; Scandura, Grazia; Mannino, Giuliana; Mele, Stefania; Sabini, Maria Gabriella; Cammarata, Francesco P.; Russo, Giorgio; Abdelhameed, Ali S.; Zappalà, Agata; Lo Furno, Debora; Giuffrida, Rosario; Li Volti, Giovanni; Tibullo, Daniele; Vicario, Nunzio; Parenti, Rosalba
- المصدر:
Cell Proliferation; Jun2024, Vol. 57 Issue 6, p1-13, 13p
- الموضوع:
- معلومة اضافية
- نبذة مختصرة :
Glioblastoma (GBM), a WHO grade IV glioma, is a malignant primary brain tumour for which combination of surgery, chemotherapy and radiotherapy is the first‐line approach despite adverse effects. Tumour microenvironment (TME) is characterized by an interplay of cells and soluble factors holding a critical role in neoplastic development. Significant pathophysiological changes have been found in GBM TME, such as glia activation and oxidative stress. Microglia play a crucial role in favouring GBM growth, representing target cells of immune escape mechanisms. Our study aims at analysing radiation‐induced effects in modulating intercellular communication and identifying the basis of protective mechanisms in radiation‐naïve GBM cells. Tumour cells were treated with conditioned media (CM) derived from 0, 2 or 15 Gy irradiated GBM cells or 0, 2 or 15 Gy irradiated human microglia. We demonstrated that irradiated microglia promote an increase of GBM cell lines proliferation through paracrine signalling. On the contrary, irradiated GBM‐derived CM affect viability, triggering cell death mechanisms. In addition, we investigated whether these processes involve mitochondrial mass, fitness and oxidative phosphorylation and how GBM cells respond at these induced alterations. Our study suggests that off‐target radiotherapy modulates microglia to support GBM proliferation and induce metabolic modifications. [ABSTRACT FROM AUTHOR]
- نبذة مختصرة :
Copyright of Cell Proliferation is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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