Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA264570 | ENA |
REPOSITORIES: ENA
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Project description:Voluntary exercise reduces the risk of cancer and lowers the risk of disease recurrence. Yet the mechanisms for this protection remain to be elucidated. Here we demonstrate that exercise halves tumor growth through an exercise-dependent mobilization and intratumoral infiltration of NK cells in malignant melanoma. Using voluntary wheel running, we show that exercise prior to and during B16 tumor challenge reduced tumor growth by 67%, and this reduction was associated with increased inflammation and immune cell infiltrates, especially NK cells, in the tumors from exercising mice. Depletion of NK cells blunted the exercise-dependent reduction in tumor growth. Moreover, during exercise, NK cells were engaged through an epinephrine-dependent mobilization to the circulation and redistributed to peripheral tissues through an IL-6 dependent mechanism. This study highlights the importance of exercise-dependent immune regulation in the control of malignant melanoma Gene expression profile of melanoma tumor tissue from two groups of exercise and non-exercise mice
2016-07-21 | E-GEOD-62628 | biostudies-arrayexpress
Project description:Voluntary exercise reduces the risk of cancer and lowers the risk of disease recurrence. Yet the mechanisms for this protection remain to be elucidated. Here we demonstrate that exercise halves tumor growth through an exercise-dependent mobilization and intratumoral infiltration of NK cells in malignant melanoma. Using voluntary wheel running, we show that exercise prior to and during B16 tumor challenge reduced tumor growth by 67%, and this reduction was associated with increased inflammation and immune cell infiltrates, especially NK cells, in the tumors from exercising mice. Depletion of NK cells blunted the exercise-dependent reduction in tumor growth. Moreover, during exercise, NK cells were engaged through an epinephrine-dependent mobilization to the circulation and redistributed to peripheral tissues through an IL-6 dependent mechanism. This study highlights the importance of exercise-dependent immune regulation in the control of malignant melanoma
2016-07-21 | GSE62628 | GEO
Project description:Physical activity reduces cancer-associated mortality through multiple mechanisms, including tumor immune microenvironment (TIME) reprogramming. However, whether and how physiological interventions promote anti-tumor immunity and immunotherapy remains elusive. Here we report that clinically relevant voluntary exercise promotes muscle-derived exosomal miR-29a-3p for extracellular matrix (ECM) degradation in patients and mouse models with multiple types of cancer, thereby permitting immune cell infiltration and immunotherapy. Mechanistically, an unbiased screening identified exercise-responsive exosomal miR-29a-3p that targets tumor cell and cancer associated fibroblasts to downregulate COL1A1 and reduce ECM. State-of-the-art techniques including cytometry by time-of-flight (CyTOF) demonstrated miR-29a-3p-induced TIME remodeling and immune cell infiltration. Combining immunotherapy with voluntary exercise or miR-29a-3p further increased the anti-tumor efficacy in preclinical models. Clinically, miR-29a-3p was correlated with degraded ECM and T-cell infiltration in various cancer types in patients, and correlated with immunotherapy responders. Our work reveals the novel predictive value of miR-29a-3p for immunotherapy, provides mechanistic insights into exercise-promoted anti-cancer immunity, and highlights the therapeutic potential of voluntary exercise in immunotherapy.
2024-08-12 | GSE273436 | GEO
Project description:Physical activity reduces cancer-associated mortality through multiple mechanisms, including tumor immune microenvironment (TIME) reprogramming. However, whether and how physiological interventions promote anti-tumor immunity and immunotherapy remains elusive. Here we report that clinically relevant voluntary exercise promotes muscle-derived exosomal miR-29a-3p for extracellular matrix (ECM) degradation in patients and mouse models with multiple types of cancer, thereby permitting immune cell infiltration and immunotherapy. Mechanistically, an unbiased screening identified exercise-responsive exosomal miR-29a-3p that targets tumor cell and cancer associated fibroblasts to downregulate COL1A1 and reduce ECM. State-of-the-art techniques including cytometry by time-of-flight (CyTOF) demonstrated miR-29a-3p-induced TIME remodeling and immune cell infiltration. Combining immunotherapy with voluntary exercise or miR-29a-3p further increased the anti-tumor efficacy in preclinical models. Clinically, miR-29a-3p was correlated with degraded ECM and T-cell infiltration in various cancer types in patients, and correlated with immunotherapy responders. Our work reveals the novel predictive value of miR-29a-3p for immunotherapy, provides mechanistic insights into exercise-promoted anti-cancer immunity, and highlights the therapeutic potential of voluntary exercise in immunotherapy.
2024-08-07 | GSE273831 | GEO
Project description:Effects of voluntary exercise in rat aorta. Spontaneously hypertensive rats (SHR) performed 5 weeks of voluntary exercise (wheel-cage running). Aortic tissue was collected and samples were pooled (3 aortae/chip). Aortae from running rats were compared to aortae from non-running rats.
2007-10-08 | E-GEOD-2418 | biostudies-arrayexpress
Project description:To undertake transcriptome-wide microarray analysis to develop a view of molecular adaptations that may underpin any benefit associated with the mild exercise regime of voluntary running Total RNA obtained from isolated whole hearts subjected to 7 days of voluntary exercise compared to sedentary control hearts (n=6/group).
2011-11-01 | E-GEOD-32391 | biostudies-arrayexpress
Project description:Effects of voluntary exercise in rat aorta. Spontaneously hypertensive rats (SHR) performed 5 weeks of voluntary exercise (wheel-cage running). Aortic tissue was collected and samples were pooled (3 aortae/chip). Aortae from running rats were compared to aortae from non-running rats. Keywords: parallel sample
2005-03-22 | GSE2418 | GEO
Project description:Gene profiling hippocampal mRNA from 1 week sedentary mice vs. 1 week voluntary exercise mice. Keywords: Exercise study.
2007-11-30 | GSE9565 | GEO
Project description:Natural killer (NK) cells play pivotal roles in antitumor immunity, yet their connection to tumor metabolism remains unclear. Our systematic analysis of multiomics data and survival data from colorectal cancer (CRC) patients uncovered a novel association between mitochondrial acetyl-CoA acetyltransferase 1 (ACAT1) and NK cell infiltration that influences disease progression. ACAT1, a metabolic enzyme involved in reversible conversion of acetoacetyl-CoA to two molecules of acetyl-CoA, exhibits nuclear protein acetylation activity through its translocation. Under immune stimulation, mitochondrial ACAT1 can be phosphorylated at serine 60 (S60) and enters the nucleus; however, this process is hindered in nutrient-poor tumor microenvironments. Nuclear ACAT1 directly acetylates lysine 146 of p50 (NFKB1), attenuating its DNA binding and transcriptional repression activity and thereby increasing the expression of immune-related factors, which in turn promotes NK cell recruitment and activation to suppress colorectal cancer growth. Furthermore, significant associations were found among low nuclear ACAT1 levels, decreased S60 phosphorylation, and reduced NK cell infiltration, as well as poor prognosis in CRC. Our findings reveal an unexpected function of ACAT1 as a nuclear acetyltransferase and elucidate its role in NK cell-dependent antitumor immunity through p50 acetylation.
2025-03-17 | GSE291785 | GEO
Project description:Intratumoral stimulatory dendritic cells (SDCs) play an important role in locally restimulating cytotoxic T cells and driving immune responses against cancer. However, the mechanisms that control SDC numbers remain poorly understood. In human melanoma, SDC numbers correlated with intratumoral expression of the gene encoding the cytokine FLT3LG, and we subsequently found in mouse and human tumors that this cytokine was predominantly produced by lymphocytes, notably including natural killer (NK) cells. NK cells stably formed conjugates with SDCs in the mouse tumor microenvironment (TME) and genetic and cellular ablation of NK cells in mice demonstrated their importance in regulation of SDC numbers through production of Flt3L. Although anti-PD-1 “checkpoint” immunotherapy for cancer largely targets T cells, we found that NK cells correlated with protective SDCs in human cancers, with patient responsiveness to anti-PD-1 immunotherapy, and with better overall survival. Our studies reveal that innate immune SDCs and NK cells cluster together as the best prognostic tool for T cell directed immunotherapy and that these innate cells are necessary for enhanced T cell tumor responses, suggesting this axis for novel therapies.
2018-04-14 | GSE113126 | GEO