Overexpression of RNA polymerase I specific SL1 component TAF1C induces cancer-specific gene expression in BEAS-2B cells

Purpose: Hyperactive RNA Polymerase I (Pol I) transcription and the upregulation of proteins essential for the initiation of Pol I transcription are the common features of a wide range of cancers . However, the role of Pol I transcription in the etiology of cancer remains unclear. Here, we activated Pol I transcription by overexpressing SL1 subunit TAF1C, and performed whole transcriptome analysis by RNA-Seq. Methods: Non-cancerous lung epithelial BEAS-2B cellswere transfected with empty vector (eV) and TAF1C expression vector (TAF1C) to generate stable cell lines. Total RNA was isolated from biological triplicates of eV and TAF1C BEAS-2B stable cells and used for RNA sequencing on Illumina platform. Results: The whole transcriptomics data revealed the upregulation of cancer related genes in BEAS-2B cells stably expressing TAF1C gene. Integration of whole transcriptome data revealed interactive regulatory networks between protein-coding RNAs, lncRNAs and miRNAs associated with various hallmarks of cancer. Conclusions: For the first time, we provide evidence for the global gene expression changes in response to activated Pol I transcription in the context of cancer. The regulatory networks identified in the study can further be validated as potential drug targets for cancer therapeutics RNA isolated from two eV replicates and three TAF1C replicates were used for long RNA and small RNA sequencing using Illumina platform