{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"submitter":["Florian Wegwitz"],"organism":["Homo sapiens"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-15389"],"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."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Sample 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 and","Nucleic 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."],"figure_sub":["Organization","MINSEQE Score","Assays and Data","Processed Data","MAGE-TAB Files"],"data_protocol":["Data 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 Galaxy"],"omics_type":["Metabolomics","Unknown","Transcriptomics","Genomics","Proteomics"],"instrument_platform":["DNBSEQ-G400"],"study_type":["CUT&RUN"],"species":["Homo sapiens"],"pubmed_authors":["Florian Wegwitz"],"additional_accession":[]},"is_claimable":false,"name":"Identification of tumor-promoting functions of the Homeobox family transcription factor MSX1 in cervical cancer","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.","dates":{"release":"2026-06-01T00:00:00Z","modification":"2026-06-01T01:00:51.987Z","creation":"2025-07-24T09:15:04.336Z"},"accession":"E-MTAB-15389","cross_references":{"ENA":["ERP177195"],"EFO":["EFO_0002944","EFO_0009973","EFO_0004170","EFO_0004917","EFO_0005518","EFO_0003816","EFO_0004184"]}}