<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/GSE336nnn/GSE336973/</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=GSE336973</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Col1a1 Knockdown Suppresses EMT, Migration, and Invasion of Oral Squamous Cell Carcinoma both In Vitro and In Vivo.</name><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.</description><dates><publication>2026/07/01</publication></dates><accession>GSE336973</accession><cross_references><GSM>GSM9845576</GSM><GSM>GSM9845575</GSM><GSM>GSM9845578</GSM><GSM>GSM9845577</GSM><GSM>GSM9845579</GSM><GSM>GSM9845581</GSM><GSM>GSM9845580</GSM><GSM>GSM9845582</GSM><GPL>21290</GPL><GSE>336973</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>