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Systematic investigation of mitochondrial transfer between cancer cells and T cells at single-cell resolution

ABSTRACT: Systematic investigation of mitochondrial transfer between cancer cells and T cells at single-cell resolution

PROVIDER: PRJNA986887 | ENA |

REPOSITORIES: ENA

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Systematic investigation of mitochondrial transfer between cancer cells and T cells at single-cell resolution

Project description:Mitochondrion (MT) as the energy-producing organelle participates in most metabolic activities of mammalian cells. Unidirectional mitochondrial transfer from T cells to cancer cells was recently observed “metabolically empowering” cancer cells while “depleting immune cells”, providing new insights into Tumor-T cell interaction and immune evasion. Here, we leveraged the increasingly adopted single-cell RNA-seq technology and introduced MERCI, a statistical deconvolution method for tracing and quantifying the process of mitochondrial trafficking between cancer and T cells. MERCI was benchmarked using data generated from a coculture system of MT-labeled cancer and T cells to accurately predict the recipient cells and their mitochondrial compositions. We independently demonstrated the cellular MT transfer signals and validated the MERCI performance by additionally generating a gold-standard mtscATAC-seq dataset. Application of MERCI to single cell human cancer samples identified a novel MT transfer phenotype and its signature genes involved in cytoskeleton remodeling, energy production and TNFα signaling pathways. Application of MERCI to ovarian cancer spatial transcriptomes revealed the prevalence of MT transfer in the tumor tissue of high T cell infiltration, which is elevated in the endothelium-rich regions. Finally, MT transfer is associated with high cell cycle activity and poor clinical outcome in our pan-cancer analysis through MERCI. In summary, MERCI enabled systematic investigation of a novel aspect of Tumor-T cell interaction and revealed MT-transfer related genes and pathways that may lead to new therapeutic opportunities.

2024-06-21 | GSE235675 | GEO

Systematic investigation of allelic regulatory activity of schizophrenia-associated common variants

Project description:Systematic investigation of allelic regulatory activity of schizophrenia-associated common variants

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Mesenchymal Stem Cells Transfer Mitochondria to the Cells with Virtually Absent Mitochondrial Function but Not to the Cells Harboring Pathogenic Mitochondrial DNA Mutations

Project description:It has been reported that human mesenchymal stem cells (MSCs) can transfer mitochondria to the cells with severely compromised mitochondrial function. We tested whether MSCs transfer mitochondria to the cells under several different conditions of mitochondrial dysfunction, including human pathogenic mitochondrial DNA (mtDNA) mutations. Using biochemical selection methods, we found that exponentially growing cells in restrictive media (uridine and bromodeoxyuridine [BrdU]+) after coculture of MSCs (uridine-independent and BrdU-sensitive) and 143B-derived cells with severe mitochondrial dysfunction induced by either long-term ethidium bromide treatment or short-term rhodamine 6G (R6G) treatment (uridine-dependent but BrdU-resistant). The exponentially growing cells had nuclear DNA fingerprint patterns identical to 143B, and a sequence of mtDNA identical to the MSCs. Since R6G causes rapid and irreversible damage to mitochondria without the removal of mtDNA, the mitochondrial function appears to be restored through a direct transfer of mitochondria rather than mtDNA alone. Conditioned media, which were prepared by treating mtDNA-less 143B 0 cells under uridine-free condition, induced increased chemotaxis in MSC, which was also supported by transcriptome analysis. A chemotaxis inhibitory agent blocked mitochondrial transfer phenomenon in the above condition. However, we could not find any evidence of mitochondrial transfer to the cells harboring human pathogenic mtDNA mutations (A3243G mutation or 4,977 bp deletion). Thus, the mitochondrial transfer is limited to the condition of a near total absence of mitochondrial function. Elucidation of the mechanism of mitochondrial transfer will help us create a potential “cell therapy-based mitochondrial restoration or mitochondrial gene therapy” for human diseases caused by mitochondrial dysfunction. time series

2011-11-22 | E-GEOD-33831 | biostudies-arrayexpress

A chemoenzymatic method for systematic investigation of the dynamics for proteins with N-terminal glycine

Project description:A systematic investigation for the dynamics of proteins with N-terminal glycine using MS-based proteomics

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Investigation of Thymic TCRd+ cells

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Mesenchymal Stem Cells Transfer Mitochondria to the Cells with Virtually Absent Mitochondrial Function but Not to the Cells Harboring Pathogenic Mitochondrial DNA Mutations

Project description:It has been reported that human mesenchymal stem cells (MSCs) can transfer mitochondria to the cells with severely compromised mitochondrial function. We tested whether MSCs transfer mitochondria to the cells under several different conditions of mitochondrial dysfunction, including human pathogenic mitochondrial DNA (mtDNA) mutations. Using biochemical selection methods, we found that exponentially growing cells in restrictive media (uridine- and bromodeoxyuridine [BrdU]+) after coculture of MSCs (uridine-independent and BrdU-sensitive) and 143B-derived cells with severe mitochondrial dysfunction induced by either long-term ethidium bromide treatment or short-term rhodamine 6G (R6G) treatment (uridine-dependent but BrdU-resistant). The exponentially growing cells had nuclear DNA fingerprint patterns identical to 143B, and a sequence of mtDNA identical to the MSCs. Since R6G causes rapid and irreversible damage to mitochondria without the removal of mtDNA, the mitochondrial function appears to be restored through a direct transfer of mitochondria rather than mtDNA alone. Conditioned media, which were prepared by treating mtDNA-less 143B rho0 cells under uridine-free condition, induced increased chemotaxis in MSC, which was also supported by transcriptome analysis. A chemotaxis inhibitory agent blocked mitochondrial transfer phenomenon in the above condition. However, we could not find any evidence of mitochondrial transfer to the cells harboring human pathogenic mtDNA mutations (A3243G mutation or 4,977 bp deletion). Thus, the mitochondrial transfer is limited to the condition of a near total absence of mitochondrial function. Elucidation of the mechanism of mitochondrial transfer will help us create a potential “cell therapy-based mitochondrial restoration or mitochondrial gene therapy” for human diseases caused by mitochondrial dysfunction.

2011-11-22 | GSE33831 | GEO

Horizontal mitochondrial transfer from microenvironment increases glioblastoma tumorigenicity

Project description:Glioblastoma (GBM) cells acquire mitochondria from glial cells in vitro and in vivo. This transfer is accompanied by increased tumor-initiation capacity.

2021-08-31 | GSE183004 | GEO

Mitochondrial regulation of bone homeostasis via mitochondria transfer [RNA-seq]

Project description:Recent studies have demonstrated that mitochondria can be transferred between different cell types to control metabolic homeostasis. However, whether the mitochondria transfer network occurred in the skeletal system or regulate skeletal metabolic homeostasis in vivo is not fully elucidated. Herein, we found that osteolineage cells transfer mitochondria to CD11b+ myeloid, B220+ lymphoid and hematopoietic stem and progenitor cells (HSPCs), of which monocytes/macrophages received the most transferred mitochondria. This process was inhibited by GC treatment contributing to the progression of glucocorticoid-induced osteoporosis (GIOP). Further analysis demonstrated that osteolineage cells transfer mitochondria to osteoclastic lineage cells via Miro1 mediated direct contact, and altered the glutathione metabolism, leading to the ferroptosis of osteoclastic lineage cells, thus inhibiting osteoclast activities. These findings revealed an unappreciated mechanism of mitochondrial regulation of skeletal metabolic homeostasis via mitochondria transfer and provide new insights of the mechanism of GIOP progression.

2024-04-08 | GSE225414 | GEO

Regulation of blood-brain barrier by astrocyte through mitochondrial transfer.

Project description:Previous data revealed the role of Mfn2 in mediating mitochondrial transfer from a subset of astrocytes that express Dmp1 to cerebrovascular endothelial cells. We used scRNA-seq to investigate the role of Mfn2-mediated mitochondrial transfer in endothelial cell functions.

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