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 Overall design: RNA isolated from two eV replicates and three TAF1C replicates were used for long RNA and small RNA sequencing using Illumina platform