biostudies-arrayexpressFlorian WegwitzHomo sapienshttps://www.ebi.ac.uk/biostudies/studies/E-MTAB-15389Cervical 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.biostudies-arrayexpressSample Collection - All steps follow the ChIC/CUT&RUN Assay Kit (Active Motif; Catalog No. 53180) protocol. Birefly: cells (500,000) are pelleted by centrifugation (600 x g, 3 min, RT), supernatant discarded. Nuclei are isolated by resuspending pellets in 100 μL Complete Nuclei Isolation Buffer (Nuclei Isolation Buffer + Protease Inhibitor Cocktail + Spermidine), incubating on ice (10 min), and repeating centrifugation (600 x g, 3 min, RT).Sequencing - Libraries were sequenced at the BGI facility in Poland using the DNBSEQ-G400 platform. The sequencing method utilized was paired-end (PE), with read lengths of 100 bases for the first and second read, and 10 bases each for the index.Library Construction - Next-generation sequencing library was prepared using the KAPA Hyper Prep Kit (KR0961–v6.17) according to the manufacturer’s instructions andNucleic Acid Extraction - All steps follow the ChIC/CUT&RUN Assay Kit (Active Motif; Catalog No. 53180) protocol. Birefly: cells/nuclei are washed twice in Complete Dig-Wash Buffer, resuspended with Concanavalin A beads, and incubated with antibody overnight at 4°C. pAG-MNase is added, followed by washes and chromatin digestion with CaCl2, then DNA is purified using DNA Purification Columns and eluted.OrganizationMINSEQE ScoreAssays and DataProcessed DataMAGE-TAB FilesData Transformation - PCR duplicates were removed using the RmDup tool (version 2.0.1). Sequencing data were normalized and differential regulated regions were identified using the Diffbind tool (v3.14.0).Sequence Alignment - Quality control of fastq files was carried out via FastQC and reads were mapped to the human reference genome (hg38) using Bowtie2 (version 2.3.4.2) on GalaxyMetabolomicsUnknownTranscriptomicsGenomicsProteomicsDNBSEQ-G400CUT&RUNHomo sapiensFlorian WegwitzfalseIdentification of tumor-promoting functions of the Homeobox family transcription factor MSX1 in cervical cancerCervical 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.2026-06-01T00:00:00Z2026-06-01T01:00:51.987Z2025-07-24T09:15:04.336ZE-MTAB-15389ERP177195EFO_0002944EFO_0009973EFO_0004170EFO_0004917EFO_0005518EFO_0003816EFO_0004184