The tumor microenvironment (TME) controls many aspects of cancer development but little is known about its effect in Glioblastoma (GBM), the main brain tumor in adults. Tumor-activated stromal cell (TASC) population, a component of TME in GBM, was induced in vitro by incubation of MSCs with culture media conditioned by primary cultures of GBM under 3D/organoid conditions. We observed mitochondrial transfer by Tunneling Nanotubes (TNT), extracellular vesicles (EV) and cannibalism from the TASC to GBM and analyzed its effect on both proliferation and survival. We created primary cultures of GBM or TASC in which we have eliminated mitochondrial DNA [Rho 0 (ρ⁰) cells]. We found that TASC, as described in other cancers, increased GBM proliferation and resistance to standard treatments (radiotherapy and chemotherapy). We analyzed the incorporation of purified mitochondria by ρ⁰ and ρ⁺ cells and a derived mathematical model taught us that ρ⁺ cells incorporate more rapidly pure mitochondria than ρ⁰ cells.

肿瘤微环境（TME）控制着癌症发展的许多方面，但其对成胶质母细胞瘤（GBM）（成人主要脑部肿瘤）的作用知之甚少。通过在3D /有机体条件下将MSC与以GBM的原代培养为条件的培养基孵育，在体外诱导肿瘤激活的基质细胞（TASC）群体（GBM中的TME成分）。我们观察了通过隧道纳米管（TNT），细胞外囊泡（EV）和食人性从TASC到GBM的线粒体转移，并分析了其对增殖和存活的影响。我们创造了我们已经消除线粒体DNA GBM或TASC的原代培养[0的Rho（ρ ⁰） 细胞]。我们发现，正如其他癌症中所述，TASC增加了GBM的增殖和对标准治疗（放射疗法和化学疗法）的抵抗力。我们通过分析纯化的线粒体的掺入ρ ⁰和ρ ⁺细胞和派生数学模型教导我们，ρ ⁺细胞结合更迅速纯线粒体比ρ ⁰细胞。