{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336973/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE336973"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Col1a1 Knockdown Suppresses EMT, Migration, and Invasion of Oral Squamous Cell Carcinoma both In Vitro and In Vivo.","description":"Oral squamous cell carcinoma (OSCC) is a lethal malignancy characterized by frequent metastasis. Utilizing a 4-NQO-induced murine model and single-cell RNA sequencing, we identified a distinct Collagen Type I Alpha 1 Chain (Col1a1+) epithelial subpopulation that is significantly expanded in OSCC, exhibits the highest epithelial-mesenchymal transition (EMT) signature, and correlates with poor patient survival. Functional studies demonstrated that Col1a1 knockdown in OSCC cell lines (HSC3) attenuated TGF-β-induced EMT, impaired migration and invasion in vitro, and reduced tumor burden in a conditional knockout mouse model. Transcriptomic profiling following Col1a1 silencing revealed the suppression of TGF-β signaling and ECM-receptor interaction pathways. We further identified BMP1 as a key downstream effector, demonstrating a direct physical interaction between COL1A1 and BMP1, and showed that COL1A1 potentiates BMP1's proteolytic activity. Rescue experiments confirmed that BMP1 is essential for COL1A1-driven tumor growth, metastasis, and TGF-β pathway activation in vivo. Furthermore, we uncovered an immunomodulatory role for the COL1A1-BMP1 axis, whereby it promotes M2 macrophage polarization via TGF-β secretion to foster an immunosuppressive tumor microenvironment. This effect was reversible using either BMP1 knockdown or TGF-β neutralization. In conclusion, our study establishes a novel COL1A1-BMP1-TGF-β signaling cascade that drives OSCC progression by autonomously enhancing tumor cell malignancy and non-autonomously reprogramming the immune landscape, nominating this axis as a promising therapeutic target.","dates":{"publication":"2026/07/01"},"accession":"GSE336973","cross_references":{"GSM":["GSM9845576","GSM9845575","GSM9845578","GSM9845577","GSM9845579","GSM9845581","GSM9845580","GSM9845582"],"GPL":["21290"],"GSE":["336973"],"taxon":["Homo sapiens"]}}