Evolution of a transplantable cancer by adaptation [CTVT_RNAseq_cells]
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PROVIDER: PRJNA1219969 | ENA |
REPOSITORIES: ENA
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Project description:Evolution of a transplantable cancer by adaptation
| PRJNA1219570 | ENA
Project description:The histocompatibility barrier prevents transmission of both normal and tumour cells between individuals 1, however clonally transmissible cancers in dogs, Tasmania devils and soft-shell clams can naturally transmit as allografts 2. To understand how tumours can escape the histocompatibility barrier, we have serially passaged a mouse melanoma first into syngeneic mice and then into progressively more mismatched mouse strains until a fully allo-transplantable tumour emerged. Here we show that tumour passaging selected for cells with an anti-viral inflammatory signature, characterised by expression of MHC-I, PD-L1, Qa-1 non-classical MHC molecules and the upregulation of intergenic endogenous retroviral elements (ERVs). Knock-out of RNA sensor RIG-I 3 in the transplantable tumour cells resulted in reduced expression of MHC-I, PD-L1 and Qa-1. Antibody-mediated blockade of both PD-L1 and Qa-1 induced tumour regression after transplantation. A similar inflammatory signature was found in human melanomas that respond to anti-PD1 antibody treatment. Thus, an inflammatory anti-viral signature likely induced by RIG-I sensing of ERVs facilitates escape of the mouse melanoma from allogeneic rejection. The results underscore the immunological plasticity of melanoma and reveal an unanticipated role for inflammation in allograft immune evasion.
2025-07-29 | GSE288825 | GEO
Project description:The histocompatibility barrier prevents transmission of both normal and tumour cells between individuals 1, however clonally transmissible cancers in dogs, Tasmania devils and soft-shell clams can naturally transmit as allografts 2. To understand how tumours can escape the histocompatibility barrier, we have serially passaged a mouse melanoma first into syngeneic mice and then into progressively more mismatched mouse strains until a fully allo-transplantable tumour emerged. Here we show that tumour passaging selected for cells with an anti-viral inflammatory signature, characterised by expression of MHC-I, PD-L1, Qa-1 non-classical MHC molecules and the upregulation of intergenic endogenous retroviral elements (ERVs). Knock-out of RNA sensor RIG-I 3 in the transplantable tumour cells resulted in reduced expression of MHC-I, PD-L1 and Qa-1. Antibody-mediated blockade of both PD-L1 and Qa-1 induced tumour regression after transplantation. A similar inflammatory signature was found in human melanomas that respond to anti-PD1 antibody treatment. Thus, an inflammatory anti-viral signature likely induced by RIG-I sensing of ERVs facilitates escape of the mouse melanoma from allogeneic rejection. The results underscore the immunological plasticity of melanoma and reveal an unanticipated role for inflammation in allograft immune evasion.
2025-07-29 | GSE288897 | GEO
Project description:Acid adaptation is a prominent event in solid tumor evolution and progression. Using RNA sequencing we studied the effect of acid adaptation on breast cancer cell line (MCF7)
2020-02-18 | GSE145383 | GEO
Project description:Experimental evolution is a powerful approach to study how ecological forces shape microbial genotypes and phenotypes, but to date strains were predominantly adapted to conditions specific to laboratory environments. The lactic acid bacterium Lactococcus lactis naturally occurs on plants and in the dairy environment and it is generally believed, that dairy strains originate from the plant niche. Here we investigated the adaptive process from the plant to the dairy niche and show that during the experimental evolution of a L. lactis plant isolate in milk, several mutations are selected that affect amino acid metabolism and transport. Three independently evolved strains were characterized by whole genome re-sequencing, revealing 4 to 28 mutational changes in the individual strains. Two of the adapted strains showed clearly increased acidification rates and yields in milk, and contained three identical point mutations. Transcriptome profiling and extensive phenotyping of the wild-type plant isolate compared to the evolved mutants, and a "natural" dairy isolate confirmed that major physiological changes associated with improved performance in the dairy environment relate to nitrogen metabolism. The deletion of a putative transposable element led to a significant decrease of the mutation rate in two of the adapted strains. These results specify the adaptation of a L. lactis strain isolated from mung bean sprouts to growth in milk and they demonstrate that niche-specific adaptations found in environmental microbes can be reproduced by experimental evolution. Multiple loop design with 12 samples and 16 dual label arrays. Each sample is hybrdized at least on two different arrays and with both dyes.
2010-06-24 | E-GEOD-20373 | biostudies-arrayexpress
Project description:Defenses against oxidants are crucial for the virulence of pathogens, with superoxide scavenging enzymes (SOSEs) playing a vital role for most aerobes. However, our knowledge of superoxide adaptation primarily stems from the study of SOSE-encoding bacteria. Here, we investigated the evolution of a naturally SOSE-deficient pathogen (Leptospira spp.), along with the alternative mechanisms it recruits to combat superoxide stress. We demonstrate that emergence of pathogenic Leptospira correlated with SOD loss, but that a long-lasting adaptation to superoxide remains possible. We reveal that cysteine and leucine biosynthesis are the most induced pathways in response to superoxide and demonstrate the importance of sulfur metabolism in superoxide adaptation in this SOSE-deficient model. We also propose cysteine oxidation as a key mediator of superoxide toxicity in the absence of SOSEs. This study challenges our conventional understanding of the oxygen toxicity theory and proposes a new model of superoxide adaptation through metabolic rewiring in bacteria.
2025-07-15 | GSE278513 | GEO
Project description:Defenses against oxidants are crucial for the virulence of pathogens, with superoxide scavenging enzymes (SOSEs) playing a vital role for most aerobes. However, our knowledge of superoxide adaptation primarily stems from the study of SOSE-encoding bacteria. Here, we investigated the evolution of a naturally SOSE-deficient pathogen (Leptospira spp.), along with the alternative mechanisms it recruits to combat superoxide stress. We demonstrate that emergence of pathogenic Leptospira correlated with SOD loss, but that a long-lasting adaptation to superoxide remains possible. We reveal that cysteine and leucine biosynthesis are the most induced pathways in response to superoxide and demonstrate the importance of sulfur metabolism in superoxide adaptation in this SOSE-deficient model. We also propose cysteine oxidation as a key mediator of superoxide toxicity in the absence of SOSEs. This study challenges our conventional understanding of the oxygen toxicity theory and proposes a new model of superoxide adaptation through metabolic rewiring in bacteria.
2025-07-15 | GSE278514 | GEO
Project description:The mechanism of evolution in different conditions can be examined from various molecular aspects that constitute a cell, namely, transcript, protein or metabolite abundance. We have analyzed transcript and metabolite abundance changes in evolved and ancestor strains in three different evolutionary conditions, namely, excess-nutrient adaptation, prolonged stationary phase adaptation and adaptation due to environmental shift, in two different strains of Escherichia coli K-12 (MG1655 and DH10B).
2007-10-02 | E-MEXP-1166 | biostudies-arrayexpress
Project description:Integrative Genomic Analyses of Human Evolution and Adaptation in Africa
| PRJNA808481 | ENA