<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/GSE297nnn/GSE297180/</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=GSE297180</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Magnetic Field Suppresses Non-Small Cell Lung Cancer via RSRP1-Mediated Secretory Signaling Axis</name><description>Magnetic field therapy holds promise for tumor treatment, yet its underlying mechanisms remain controversial. The traditional ROS theory fails to fully explain the observed magnetic field-induced inhibition. Building on prior findings, we identified the key target of magnetic field-mediated tumor suppression and established a magnetic inhibition model. Integrative multi-omics analysis (transcriptome + proteome) of 293T and A549 cells exposed to (5 mT, 20 Hz) magnetic fields pinpointed RSRP1 as a critical molecular target. We experimentally validated RSRP1's essential role using CRISPR-Cas9-mediated gene disruption and TET-on inducible expression systems. Proteomic analysis revealed that magnetic field exposure (5 mT, 20 Hz) induced >200-fold upregulation of RSRP1 protein in both non-tumorigenic 293T and tumorigenic A549 cells. CRISPR-Cas9-mediated RSRP1 knockout completely abolished A549 cells' responsiveness to magnetic fields. Notably, restoring RSRP1 expression via a doxycycline-inducible system reinstated magnetic field-induced secretion of inhibitory factors, with conditioned media from exposed cells significantly inhibiting naive tumor cell proliferation (p&lt;0.05). Magnetic field (5 mT, 20 Hz) exposure transcriptionally upregulated RSRP1 endogenously, as confirmed by transcriptomic and qPCR analyses, while exogenously overexpressed RSRP1 via a doxycycline-inducible system remained unresponsive, indicating that magnetic regulation requires endogenous transcriptional control. This study establishes a "magnetic field→RSRP1→secretory factor→target response" cascade, providing a transformative framework for non-invasive tumor therapy.</description><dates><publication>2026/05/12</publication></dates><accession>GSE297180</accession><cross_references><GSM>GSM8985070</GSM><GSM>GSM8985071</GSM><GSM>GSM8985072</GSM><GSM>GSM8985073</GSM><GPL>29480</GPL><GSE>297180</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>