TSSC4 inhibits tumor cell growth by modulating the alternative splicing and expression of tumor-associated genes
Post-transcriptional regulation encompasses the regulation of gene expression at the RNA level following transcription. This regulation involves a series of modifications and processing events that occur to the gene transcripts in eukaryotic cells. These processes include splicing, editing, stabilization and degradation of RNA, which collectively ensure the precise control of gene expression. TSSC4 (tumor suppressing subtransferable candidate 4) is a component of U5 snRNP, which associates with U5 snRNP and the PRPF19 complex. It has been reported that TSSC4 inhibits cancer cell proliferation and tumor growth. Here, our findings indicate that TSSC4 deficiency results in widespread alterations in gene expression and splicing patterns. Knockout of TSSC4 is found to enhance the proliferation of cancer cells driven by oncogene. In conclusion, our results provided evidence that the potential importance of TSSC4 in mediating cancer progression, highlighting its role as a critical mediator of gene expression and splicing in tumor biology Overall design: To further investigate how TSSC4 affects  tumor cell growth, we utilized CRISPR/Cas9  to knock out TSSC4 in HeLa cells. Infect cells with lentiCRISPR-Cas9 lentivirus. After 48 hours, add 2 µg/ml puromycin to select for transduced cells, and select and expand single-cell clones. Comparative gene expression and alternative splicing profiling analysis of RNA-seq data for TSSC4 knockout and WT HeLa cells.