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Dynamic magneto-mechanical force in lysosomes instructs durable macrophage repolarization for antitumor immunity

ABSTRACT: Mechanical forces are the emerging physical cue to regulate biochemical signals of immune cells for antitumor immunity. Here we used single RNA sequencing to analyze the activations of different immune cells in tumor tissue after treated by magneto-mechanical force.

ORGANISM(S): Mus musculus

PROVIDER: GSE275018 | GEO | 2025/08/16

REPOSITORIES: GEO

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Dynamic magneto-mechanical force in lysosomes instructs durable macrophage repolarization for antitumor immunity.

Project description:Mechanical forces are the emerging physical cue to regulate biochemical signals of immune cells for antitumor immunity. Here, we develop a magneto-mechanical force-triggered lysosomal membrane permeabilization (MagLMP) strategy to dictate durable macrophage repolarization, which leads to dynamic damage of lysosomal membrane via the finely tuned torque-induced vortex. We found that the MagLMP could activate M1-like macrophage repolarization, followed by the mounting of antitumor immunity. Together, we establish an intracellular mechanical strategy to dynamically manipulate innate immune responses in vivo and provide the tool for durable immunotherapy through organelle mechanotransduction.

2025-08-01 | GSE273977 | GEO

Dynamic magneto-mechanical force in lysosomes instructs durable macrophage repolarization for antitumor immunity

Project description:Dynamic magneto-mechanical force in lysosomes instructs durable macrophage repolarization for antitumor immunity

| PRJNA1148975 | ENA

Dynamic magneto-mechanical force in lysosomes instructs durable macrophage repolarization for antitumor immunity.

Project description:Dynamic magneto-mechanical force in lysosomes instructs durable macrophage repolarization for antitumor immunity.

| PRJNA1144398 | ENA

Breast tumor stiffness instructs bone metastasis via mechanical memory

Project description:The mechanical microenvironment of primary breast tumors plays a substantial role in promoting tumor progression. While the transitory response of cancer cells to pathological stiffness in their native microenvironment has been well described, it is unclear whether mechanical stimuli in the primary tumor influence distant, late-stage metastatic phenotypes in absentia. Here, we show that primary tumor stiffness promotes stable yet non-genetically heritable phenotypes in breast cancer cells. This “mechanical memory” instructs cancer cells to adopt and maintain increased cytoskeletal dynamics, traction force, and 3D invasion in vitro, in addition to promoting osteolytic bone metastasis in vivo. We established a “mechanical conditioning score” comprised of mechanically-regulated genes as a proxy measurement of tumor stiffness response, and we show that it is associated with bone metastasis in patients. Using a discovery approach, we mechanistically traced mechanical memory in part to ERK-mediated mechanotransductive activation of RUNX2, an osteogenic gene bookmarker and bone metastasis driver. This combination of traits allows for the stable transactivation of osteolytic target genes which persists after cancer cells disseminate from their activating microenvironment. Using genetic, epigenetic, and functional approaches, RUNX2-mediated mechanical memory can be stimulated, repressed, selected, or extended. In concert with previous studies detailing how biochemical properties of the primary tumor stroma influence distinct metastatic phenotypes, the impact of local biomechanical properties we present here support a generalized model of cancer progression in which the integrated properties of the primary tumor microenvironment govern cell behavior in the metastatic microenvironment.

2021-07-01 | GSE127887 | GEO

Project description:The aging process significantly alters the biomechanical properties of fibroblasts, impacting their cytoskeletal and chromatin organization. These changes are pivotal in modulating cellular responses to mechanical and biochemical stimuli. This study investigates the hypothesis that aging leads to fibroblasts’ divergent adaptation mechanisms to external stimuli. Herein, fibroblasts from young and old cohorts were embedded in 3D collagen gels and subjected to tension force alone (tension stimulus) or tension +/- Transforming Growth Factor beta (TGFb) (tension/TGFb stimuli). The study revealed that mechanical forces and aging exert profound effects on chromatin architecture. Young cells adapted more rapidly to mechanical stress and showed a heightened responsiveness to TGFβ compared to older cells. The identification of key transcription factors implicated in age-dependent responses was further examined, assessing their potential in cellular rejuvenation.

2026-03-15 | GSE300230 | GEO

Fibroblast-specific focal adhesion kinase links mechanical force to fibrosis via chemokine-mediated inflammatory pathways

Project description:Hypertrophic scar (HTS) formation is characterized by exuberant fibroproliferation for reasons that remain poorly understood1. One important but often overlooked component of wound repair is mechanical force, which regulates reciprocal cell-matrix interactions through focal adhesion components including focal adhesion kinase (FAK)1,2. Here we report that FAK is activated following cutaneous injury and that this activation is potentiated by mechanical loading. Transgenic mice lacking fibroblast-specific FAK exhibit significantly less fibrosis in a preclinical model of HTS formation. Inflammatory pathways involving monocyte chemoattractant protein-1 (MCP-1), a chemokine highly implicated in human skin fibrosis3, are triggered following FAK activation, mechanistically linking physical force to fibrosis. Further, small molecule inhibition of FAK effectively abrogates fibroproliferative mechanisms in human cells and significantly reduces scar formation in vivo. Collectively, these findings establish a molecular basis for HTS formation based on the mechanical activation of fibroblast-specific FAK and demonstrate the therapeutic potential of targeted mechanomodulatory strategies. Wildtype murine tissue was harvested at either day 6 or 14 post-injury following 48 hours or 10 days of mechanical loading, respectively (n=4 mice per group per time point). Murine RNA was isolated, labeled, and hybridized to the GeneChip microarray according to the manufacturer’s protocols (Affymetrix, Santa Clara, CA, USA). Each gene in the microarray was represented by 20 oligonucleotide pairs, with each pair consisting of an oligonucleotide perfectly matched to the cDNA sequence, and a second oligonucleotide containing a single base mismatch. Raw microarray data (sample intensity files) were processed using GeneSpring GX 11.0 (Agilent Technologies Inc., Santa Clara, CA, USA).

2011-01-14 | E-GEOD-26390 | biostudies-arrayexpress

Mechanical force induces rapid phosphorylation-dependent signaling in Xenopus embryos

Project description:We inegrated quantitative phosphoproteome, proteome, a tergeted MS analysis, in conjunction with pathway perturbation to obtain a global view of the mechano-responses of embryonic tissues. This study provides mechanistic insights into mechanical force sensing pathways.

2019-10-09 | MSV000084444 | MassIVE

Mechanical force induces rapid phosphorylation-dependent signaling in Xenopus embryos

2019-02-16 | PXD010676 | Pride

Project description:The aging process significantly alters the biomechanical properties of fibroblasts, impacting their cytoskeletal and chromatin organization. These changes are pivotal in modulating cellular responses to mechanical and biochemical stimuli. This study investigates the hypothesis that aging leads to fibroblasts’ divergent adaptation mechanisms to external stimuli. Herein, fibroblasts from young and old cohorts were embedded in 3D collagen gels and subjected to tension and Transforming Growth Factor beta (TGFb) stimulation. The study revealed that mechanical forces and aging exert profound effects on chromatin architecture. Young cells adapted more rapidly to mechanical stress and showed a heightened responsiveness to TGFβ compared to older cells. The identification of key transcription factors implicated in age-dependent responses was further examined, assessing their potential in cellular rejuvenation.

2026-03-27 | GSE300231 | GEO

Mechanical force promotes dimethylarginine dimethylaminohydrolase 1-mediated hydrolysis of the metabolite asymmetric dimethylarginine to enhance bone formation

Project description:<p>Mechanical force is critical for the development and remodeling of bone. Here we report that mechanical force regulates the production of the metabolite asymmetric dimethylarginine (ADMA) via regulating the hydrolytic enzyme dimethylarginine dimethylaminohydrolase 1 (Ddah1) expression in osteoblasts. The presence of -394 4N del/ins polymorphism of Ddah1 and higher serum ADMA concentration are negatively associated with bone mineral density. Global or osteoblast-specific deletion of Ddah1 leads to increased ADMA level but reduced bone formation. Further molecular study unveils that mechanical stimulation enhances TAZ/SMAD4-induced Ddah1 transcription. Deletion of Ddah1 in osteoblast-lineage cells fails to respond to mechanical stimulus-associated bone formation. Taken together, the study reveals mechanical force is capable of down-regulating ADMA to enhance bone formation.</p>

2021-11-23 | MTBLS3725 | MetaboLights

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