Lineage-Specific Oncogenic Reprogramming of COL17A1 Orchestrates a Pro-Invasive and Hypoxia-Adapted Niche in HNSC

Head and Neck Squamous Cell Carcinoma (HNSC) originates from specialized epithelium, and identifying lineage-specific oncogenes is crucial for understanding tumor progression. In this study, we identified COL17A1 as a potential core regulator in HNSC. To characterize the transcriptional landscape and molecular mechanisms regulated by COL17A1, we performed bulk RNA-sequencing on the human oral squamous cell carcinoma cell line, SAS. We compared the gene expression profiles of control cells (transfected with negative control siRNA) against COL17A1-depleted cells (transfected with COL17A1-specific siRNAs). This dataset reveals that depletion of COL17A1 leads to the dismantlement of a specific "Partial-EMT" gene module and induces a metabolic shift, highlighting its role in maintaining the malignant phenotype of HNSC cells. Overall design: SAS cells were cultured and transfected with either a negative control siRNA (NC) or a specific siRNA targeting COL17A1 (siRNA sequence #2). Total RNA was extracted post-transfection. Messenger RNA libraries were prepared and sequenced on the Illumina NovaSeq platform to generate paired-end reads. The experiment consists of 2 samples: one negative control sample and one COL17A1-knockdown sample.