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Voluntary exercise suppresses tumor growth through exercise-directed recruitment and intratumoral infiltration of NK cells

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE62628 | GEO | 2016/07/21

SECONDARY ACCESSION(S): PRJNA264570

REPOSITORIES: GEO

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Voluntary exercise suppresses tumor growth through exercise-directed recruitment and intratumoral infiltration of NK cells

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

Analysis of SAMP8 and SAMR1 mice after an exercise intervention

Project description:Microarrays have been used to analyze the effect of voluntary wheel running in the SAMP8 mice using the SAMR1 mouse strain as control. Hippocampal gene expresion of SAMP8 which have been resting or exercising and SAMR1 sedentary.

2012-03-20 | E-GEOD-36571 | biostudies-arrayexpress

Mouse HiRIEF LCMS Proteomics - Sedentary VS Exercise, WT VS PolgA mutant

Project description:Mitochondrial dysfunction is implicated in aging and aging-related disorders, such as neurodegenerative diseases and stroke. To study the effects of progressive mitochondrial dysfunction, a homozygous knock-in mouse expressing a proof-reading deficient version of the nucleus-encoded catalytic subunit of mitochondrial DNA (mtDNA) polymerase (PolgA) has been developed. In the mtDNA mutator mouse the proofreading activity of PolgA has been abolished by a single amino acid change. PolgA is the catalytic subunit of the polymerase gamma, which is involved in replicating and proofreading the mitochondrial DNA. As a result, mtDNA mutator mice develop high levels of point mutations and linear deletions, which lead to several human-like phenotypes associated with aging, including reduced lifespan (42-44 weeks), weight loss, alopecia, anemia, kyphosis, osteoporosis, sarcopenia, loss of subcutaneous fat, and reduced fertility. We investigate the molecular mechanism through which exercise may improve the phenotype of the mtDNA mutator mouse, which is a model of premature aging induced by mitochondrial dysfunction. Remarkably, forced endurance exercise has been shown to rescue the progeroid aging phenotypes of the mtDNA mutator mice, and to induce systemic mitochondrial rejuvenation. Here, using voluntary, rather than forced exercise, we investigate the molecular mechanisms underlying such a dramatic improvement, and also assess the effect of exercise on brain tissues, such as cortex and striatum in our model. The complete proteome of key tissues (muscle, brain cortex, brain striatum) from exercising and sedentary mtDNA mutator mice as well as exercising and sedentary wild type mice is quantified using peptide high-resolution isoelectric focusing (HiRIEF) coupled with liquid chromatography tandem mass spectrometry (LC-MS/MS) with an isobaric tag (TMT10plex) strategy.

2019-08-05 | PXD011741 | Pride

Mus musculus

Project description:Voluntary exercise suppresses tumor growth through exercise-directed recruitment and intratumoral infiltration of NK cells

| PRJNA264570 | ENA

Voluntary exercise sensitizes cancer immunotherapy via collagen degradation-orchestrated inflammatory tumor immune microenvironment

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

Voluntary exercise sensitizes cancer immunotherapy via collagen degradation-orchestrated inflammatory tumor immune microenvironment

2024-08-07 | GSE273831 | GEO

Effects of acute exercise on gene expression in exercising and non-exercising human skeletal muscle

Project description:Background: Exercising is know to have an effect on exercising skeletal muscle, but unkown is the effect on non-exercising skeletal muscle. Gene expression changes in the non-exercising skeletal muscle would point to a signalling role of skeletal muscle 9 healthy middle-aged men performed 1 hour of one-legged exercise, before and afterwards muscle biopsies were taken from both legs. Skeletal muscle biopsies were analyzed by microarray.

2012-10-23 | E-GEOD-41769 | biostudies-arrayexpress

Effects of voluntary exercise in rat aorta

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

Analysis of brain cortices of SAMP8 and SAMR1 mice after an exercise intervention

Project description:Microarrays has been used to analyze the effect of voluntary wheel running in the SAMP8 mice using the SAMR1 mouse strain as control. Cortex gene expresion of SAMP8 which have been resting or exercising and SAMR1 sedentary.

2012-06-04 | E-GEOD-38465 | biostudies-arrayexpress

Timed Exercise and Clocks: Does a Minimally Functional Suprachiasmatic Clock Support 24h Behavioral Rhythms?

Project description:The brain’s suprachiasmatic nucleus (SCN) is the master clock driving circadian rhythms in mammals. Vasoactive intestinal polypeptide (VIP) and its cognate receptor, VPAC2, are expressed in SCN neurons and mice with genetically targeted deletion of VPAC2 (Vipr2 -/-animals) show aberrant resetting to light, abnormal behavioral rhythms, and diminished SCN clock gene expression. Timed daily access to a running-wheel (scheduled voluntary exercise; SVE) promotes Vipr2 -/- SCN clock cell synchrony and 24h behavioral rhythms. We hypothesized that timed exercise alters the SCN transcriptome. Here, in control (Vipr2+/+) and Vipr2-/- mice under freely exercising and SVE conditions, RNAseq and qRT-PCR were used to measured gene expression of laser-dissected SCN. Compared to Vipr2+/+ mice, hundreds of genes were differentially expressed in the SCN from Vipr2-/- mice rhythmic in the freely exercising condition. Unexpectedly, SVE did not promote a Vipr2+/+-like SCN transcriptome in Vipr2-/- mice and many transcripts involved in SCN function including Avp, C1ql3, Gpr176, Prok2, Sst, Per2, and Nr1d1 remained dysregulated in the SVE condition. By contrast, circadian oscillators in the liver and lung were mostly intact in Vipr2-/- mice. This study indicates that marked molecular deficits in the SCN are sustained in behaviorally rhythmic Vipr2-/- mice, raising the possibility that a minimal functional SCN circadian clock can underpin whole animal rhythms.

2023-01-20 | GSE207992 | GEO

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