<HashMap><database>biostudies-arrayexpress</database><scores/><additional><submitter>Florian Wegwitz</submitter><organism>Homo sapiens</organism><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-15395</full_dataset_link><description>Cervical cancer (CC) remains a major cause of cancer-related mortality, particularly in regions with limited screening access, despite being highly preventable and treatable when detected early. MSX1, a homeobox transcription factor with dual roles as a tumor suppressor and oncogene, has an unclear role in CC pathogenesis. This study reveals that MSX1 acts as a tumor-promoting factor in CC, with de novo expression observed in precancerous lesions but absent in normal cervical epithelium. MSX1 enhances clonogenicity and migrationin cervical cancer cells, driven by epithelial-to-mesenchymal transition (EMT) induction. Mechanistically, MSX1 activates RHO/RAC/CDC42 cytoskeletal signaling pathways, with FOS—a downstream RHO effector—identified as a key mediator of CC aggressiveness. Targeting RHO signaling or FOS reverses MSX1-driven aggressive phenotypes, while proteasomal degradation of MSX1 reduces chemoresistance. These findings highlight MSX1’s critical role in CC progression and suggest its potential as a therapeutic target. The study underscores MSX1’s involvement in key oncogenic pathways, offering new insights for developing targeted therapies in cervical cancer.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Sample Collection - Cells were grown in 6-well plates for 72 hours in biological triplicates.</sample_protocol><sample_protocol>Nucleic Acid Extraction - RNA was extracted using EXTRAzol® Lysis Reagent (BLIRT) according to the manufacturer's protocol.</sample_protocol><sample_protocol>Sequencing - Multiplexed libraries were adjusted to a concentration of 2 nM and sequenced on a HiSeq 4000 Illumina-Sequencer at the NGS-Integrative Genomics (NIG) at the University Medical Center Göttingen (UMG).</sample_protocol><sample_protocol>Library Construction - Libraries were prepared using TruSeq RNA Library Prep Kit v2 (Illumina®) after verifying the RNA integrity on an agarose gel. Library quality was assessed using an Agilent Bioanalyzer 2100.</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>Processed Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><data_protocol>Data Transformation - Normalization and differential gene expression was performed with DeSeq2.</data_protocol><data_protocol>Sequence Alignment - Fastq files were processed in the Galaxy environment (https://galaxy.gwdg.de) provided by the “Gesellschaft für wissenschaftliche Datenverarbeitung mbH Göttingen” (GWDG). Sequencing data were trimmed (FASTQ Trimmer tool), aligned to the human reference genome (HG38) with the HISAT2 tool and assigned to their respective genomic features using featurecounts.</data_protocol><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><instrument_platform>Illumina HiSeq 4000</instrument_platform><study_type>RNA-seq of coding RNA</study_type><species>Homo sapiens</species><pubmed_authors>Florian Wegwitz</pubmed_authors></additional><is_claimable>false</is_claimable><name>Identification of tumor-promoting functions of the Homeobox family transcription factor MSX1 in cervical cancer</name><description>Cervical cancer (CC) remains a major cause of cancer-related mortality, particularly in regions with limited screening access, despite being highly preventable and treatable when detected early. MSX1, a homeobox transcription factor with dual roles as a tumor suppressor and oncogene, has an unclear role in CC pathogenesis. This study reveals that MSX1 acts as a tumor-promoting factor in CC, with de novo expression observed in precancerous lesions but absent in normal cervical epithelium. MSX1 enhances clonogenicity and migrationin cervical cancer cells, driven by epithelial-to-mesenchymal transition (EMT) induction. Mechanistically, MSX1 activates RHO/RAC/CDC42 cytoskeletal signaling pathways, with FOS—a downstream RHO effector—identified as a key mediator of CC aggressiveness. Targeting RHO signaling or FOS reverses MSX1-driven aggressive phenotypes, while proteasomal degradation of MSX1 reduces chemoresistance. These findings highlight MSX1’s critical role in CC progression and suggest its potential as a therapeutic target. The study underscores MSX1’s involvement in key oncogenic pathways, offering new insights for developing targeted therapies in cervical cancer.</description><dates><release>2026-06-01T00:00:00Z</release><modification>2026-06-01T01:00:54.413Z</modification><creation>2025-07-24T15:10:45.166Z</creation></dates><accession>E-MTAB-15395</accession><cross_references><ENA>ERP177218</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0004917</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003816</EFO><EFO>EFO_0003738</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>