Depletion of TAFIB Gene Inhibits Ribosome Biosynthesis and Proliferation of Gastric Tumor through Enhancing c-MYC mRNA Degradation

Abstract

Abstract With population growth and aging, the number of new cases about Stomach adenocarcinoma (STAD) is expected to continue to increase in the future. Increased ribosome biosynthesis (RiBi), a hallmark of many cancers for over 100 years, as a result of an emerging target for cancer therapy. The first key step of RiBi, the transcription of RNA polymerase I (Pol I) into the precursor ribosomal RNA (pre-rRNA), needs a Pol I specific Pre-initiation Complex (PIC) for accurate recruitment. Mammalian PIC of Pol I includes selectivity factor 1 (SL1), RRN3 and upstream binding factor (UBF), of which SL1 is essential and can stabilize the PIC structure. TAF1B, TBP-associated factor 1B, is one of the component subunits of SL1. TAF1B is required for Pre-initiation Complex of RNA polymerase I, but its function in cancers is not fully understood. In this study, when we knocked down TAF1B gene in STAD ,we found that the transcription and content of c-MYC decreased, which was associated with RPL 5, RPL 11 and RISC.