Mitochondria transfer from tumor-activated stromal cells (TASC) to primary Glioblastoma cells

Salaud, Céline; Álvarez-Arenas, Arturo; Geraldo, Fanny; Belmonte-Beitia, Juan; Calvo, Gabriel F.; Gratas, Catherine; Pecqueur, Claire; Garnier, Delphine; Pérez-Garcı́a, Vı́ctor M.; Vallette, François M.; Oliver, Lisa

doi:10.1016/j.bbrc.2020.08.101

Cited by 43 publications

(44 citation statements)

References 29 publications

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“…Mitochondrial membrane potential and mitochondrial oxygen free radical were also changed. A series of abnormalities in mitochondria can activate downstream-related pathways, thereby activating the transcription of proliferation-related genes and promoting cell proliferation [ 23 , 24 ]. Reduced concentration of mitochondrial calcium can inhibit the activity of Ca2+-dependent enzymes in mitochondria, including pyruvate dehydrogenase (PDH), isocitrate dehydrogenase, α -ketoglutarate dehydrogenase, and ATP synthase, which inhibit glucose oxidation and promote glycolysis.…”

Section: Discussionmentioning

confidence: 99%

[Retracted] Curcumin Improves Pulmonary Hypertension Rats by Regulating Mitochondrial Function

Chen

Jiang

Zhu

et al. 2021

BioMed Research International

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Objective. To investigate the role of curcumin in regulating pathogenesis of pulmonary arterial smooth muscle cells (PASMCs) derived from pulmonary arterial hypertension (PAH) model. Methods. Male Sprague Dawley rats were injected with monocrotaline (MCT) to establish the PAH experimental model. The rats were divided into control group, MCT group, and curcumin group. At the end of the study, hemodynamic data were measured to determine pulmonary hypertension. Proliferation ability of PASMCs, a remodeling indicator of pulmonary artery and right ventricle, was detected. In addition, the morphology and function of mitochondria, antiglycolysis and antiproliferation pathways, and genes were also analyzed. Results. Curcumin may function by reversing MCT-mediated pulmonary vascular remodeling in rats. Curcumin effectively improved pulmonary vascular remodeling, promoted PASMC apoptosis, and protected mitochondrial function. In addition, curcumin treatment suppressed the PI3K/AKT pathway in PASMCs and regulated the expression of antiproliferative genes. Conclusion. Curcumin can improve energy metabolism and reverse the process of PAHS. However, there were side effects of curcumin in MCT-induced rats, suggesting that the dosage should be treated with caution and its toxicological mechanism should be further studied and evaluated.

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Section: Discussionmentioning

confidence: 99%

[Retracted] Curcumin Improves Pulmonary Hypertension Rats by Regulating Mitochondrial Function

Chen

Jiang

Zhu

et al. 2021

BioMed Research International

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“…We show that TNT enables mitochondria exchange and other cytoplasmic factors from the tumor cell into the non-tumor cells. Mitochondrial exchange via TNT is not a new concept, as previously published by several groups 12 , 22 , 58 , 63 . The function of the mitochondrial transfer was suggested but not demonstrated.…”

Section: Discussionmentioning

confidence: 93%

“…Third, TNT communicate the cytoplasm of two or more cells at a minimal distance of 30 µm with open-ended and non-open-ended processes. Fourth, the TNT process can branch and reach distances up to 500 µm in vivo and in vitro 13 , 22 , 23 , 105 , 107 . Fifth, TNT can transport organelles, vesicular structures, and small molecules between TNT-connected cells.…”

Section: Methodsmentioning

confidence: 99%

Tunneling nanotubes, TNT, communicate glioblastoma with surrounding non-tumor astrocytes to adapt them to hypoxic and metabolic tumor conditions

Valdebenito

Malik

Luu

et al. 2021

Sci Rep

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Cell-to-cell communication is essential for the development and proper function of multicellular systems. We and others demonstrated that tunneling nanotubes (TNT) proliferate in several pathological conditions such as HIV, cancer, and neurodegenerative diseases. However, the nature, function, and contribution of TNT to cancer pathogenesis are poorly understood. Our analyses demonstrate that TNT structures are induced between glioblastoma (GBM) cells and surrounding non-tumor astrocytes to transfer tumor-derived mitochondria. The mitochondrial transfer mediated by TNT resulted in the adaptation of non-tumor astrocytes to tumor-like metabolism and hypoxia conditions. In conclusion, TNT are an efficient cell-to-cell communication system used by cancer cells to adapt the microenvironment to the invasive nature of the tumor.

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“…In a study on ovarian cancer and breast cancer cell lines, it was demonstrated that the preferential transfer through TNT of mitochondria was from endothelial to cancer cells, demonstrating that mitochondria uptake, inducing phenotypic advantage in recipient cells, resulted in the acquisition of chemoresistance [ 128 ]. TNT mitochondrial transfer has also been linked to human tumor-activated stromal cells (TASCs) and glioblastoma cells, conferring resistance to standard treatments (radiotherapy and chemotherapy) [ 137 ]. Drug resistance in T-ALL makes this leukemia one of the most aggressive hematologic malignancies.…”

Section: Role Of Mitochondrial Remodeling (Fusion Fission Mitophagy and Transfer) In Cancer Chemoresistancementioning

confidence: 99%

Mitochondria: Insights into Crucial Features to Overcome Cancer Chemoresistance

Genovese

Carinci

Modesti

et al. 2021

IJMS

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Mitochondria are key regulators of cell survival and are involved in a plethora of mechanisms, such as metabolism, Ca2+ signaling, reactive oxygen species (ROS) production, mitophagy and mitochondrial transfer, fusion, and fission (known as mitochondrial dynamics). The tuning of these processes in pathophysiological conditions is fundamental to the balance between cell death and survival. Indeed, ROS overproduction and mitochondrial Ca2+ overload are linked to the induction of apoptosis, while the impairment of mitochondrial dynamics and metabolism can have a double-faceted role in the decision between cell survival and death. Tumorigenesis involves an intricate series of cellular impairments not yet completely clarified, and a further level of complexity is added by the onset of apoptosis resistance mechanisms in cancer cells. In the majority of cases, cancer relapse or lack of responsiveness is related to the emergence of chemoresistance, which may be due to the cooperation of several cellular protection mechanisms, often mitochondria-related. With this review, we aim to critically report the current evidence on the relationship between mitochondria and cancer chemoresistance with a particular focus on the involvement of mitochondrial dynamics, mitochondrial Ca2+ signaling, oxidative stress, and metabolism to possibly identify new approaches or targets for overcoming cancer resistance.

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Mitochondria transfer from tumor-activated stromal cells (TASC) to primary Glioblastoma cells

Cited by 43 publications

References 29 publications

[Retracted] Curcumin Improves Pulmonary Hypertension Rats by Regulating Mitochondrial Function

[Retracted] Curcumin Improves Pulmonary Hypertension Rats by Regulating Mitochondrial Function

Tunneling nanotubes, TNT, communicate glioblastoma with surrounding non-tumor astrocytes to adapt them to hypoxic and metabolic tumor conditions

Mitochondria: Insights into Crucial Features to Overcome Cancer Chemoresistance

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