<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE343nnn/GSE343051/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE343051</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Mechanical stress remodeling drives epithelial-mesenchymal transition in the tumor microenvironment</name><description>The dynamic mechanical response of tissues underlies their physiological function, yet direct, quantitative measurement of tissue stress in vivo has remained a major challenge. Here, we introduce the mechanoMR microparticle (M³) sensor, a platform that transduces local tissue mechanical stress into quantitative magnetic resonance (MR) readouts with single-particle resolution. The sensor comprises alginate hydrogel microparticles (~70 μm) homogeneously embedded with Zn₀.₄Fe₂.₆O₄ magnetic nanoparticles, where stress-induced hydrogel compression reduces local water content and restricts proton diffusion surrounding the magnetic nanoparticles, thereby modulating magnetic nanoparticle-mediated transverse relaxation (R₂). Calibration of the stress-R₂ relationship enables quantitative measurement of local tissue stress over a physiologically relevant range of 0-15 kPa. We demonstrate the platform in tumor spheroids and mouse xenografts, enabling non-invasive, spatiotemporal mapping of tissue stress during tumor progression. Using this approach, we show that epithelial-mesenchymal transition (EMT) is accompanied by distinct stress-remodeling patterns in vivo. Strikingly, abrupt stress increases, rather than cumulative or peak stress magnitude, determine EMT induction. Transcriptomic profiling reveals that gradual stress loading activates cytoprotective FOXO/AMPK pathways that reinforce epithelial stability, whereas acute stress surges overwhelm these defense mechanisms, predisposing cells to mesenchymal reprogramming. These findings establish the M3 sensor as a broadly applicable platform for linking tissue mechanics to cell-state transitions in development and disease.</description><dates><publication>2026/09/11</publication></dates><accession>GSE343051</accession><cross_references><GSM>GSM9945326</GSM><GSM>GSM9945325</GSM><GSM>GSM9945328</GSM><GSM>GSM9945327</GSM><GSM>GSM9945333</GSM><GSM>GSM9945332</GSM><GSM>GSM9945324</GSM><GSM>GSM9945335</GSM><GSM>GSM9945334</GSM><GSM>GSM9945331</GSM><GSM>GSM9945330</GSM><GSM>GSM9945329</GSM><GPL>34281</GPL><GSE>343051</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>