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Abstract
Background
Transcription factor 19 (TCF19) is an important member of the transcription factor family, but its role in cancer is not well understood. This study aims to clarify the function of TCF19 and explore its mechanisms across various cancers, with a specific focus on breast cancer, using bioinformatics analysis and histological validation.
Methods
Gene expression profiles and clinical data were obtained from sources like The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and Genotype-Tissue Expression (GTEx) for bioinformatics analysis. Tumor–immune interactions were studied using the TISIDB database for immune-related insights. To confirm these findings, TCF19 expression was measured using quantitative RT-PCR, immunohistochemistry (IHC), and western blot assays. Additional validation was done with various experimental techniques, including CCK-8, colony-forming, transwell, and cell line-derived xenograft assays.
Results
TCF19 is significantly upregulated in many cancerous tissues, including breast cancer, as confirmed across multiple datasets and clinical samples. Higher TCF19 levels were associated with a poorer prognosis. Experimentally reducing TCF19 expression in MCF-7 cells impaired key cellular functions such as proliferation, invasion, migration, and tumor formation. Pathway enrichment analysis of TCGA samples revealed a strong link between TCF19 and the PLK1 pathway, a finding further supported by western blot results showing PLK1 downregulation following TCF19 silencing.
Conclusions
High TCF19 expression is closely linked to poorer outcomes, especially in breast cancer. These findings highlight TCF19 as a promising biomarker with broad potential applications in cancer diagnosis and prognosis.