In vivo CRISPR screen identifies SNRPC as a regulator for facilitating triple-negative breast cancer progression [RNA-Seq]

In this study, we employed an in vivo CRISPR screening and a TNBC progression model to identify potentially oncogenic RBPs. We identified the small nuclear ribonucleoprotein polypeptide C (SNRPC), a subunit of the U1 small nuclear ribonucleoprotein particle (U1 snRNP), as a key modulator involved in TNBC progression. SNRPC was frequently upregulated and relevant to poor prognosis in TNBC patients. SNRPC ablation significantly impaired the proliferation, migration and invasion of TNBC cells in vitro and in vivo. In addition, SNRPC was essential for the stability of U1 snRNP and contributed to the RNA Pol II-controlled transcription program. Knockdown of SNRPC decreased RNA Pol II enrichment on some oncogenes (TNFAIP2, E2F2 and CDK4) and reduced their expression levels. We further confirmed that SNRPC deletion would inhibit TNBC progression partially through the TNFAIP2-Rac1-β-catenin signal. Comparative gene expression profling analysis of RNA-seq data for MCF10 CA1a cell and its SNRPC-KD dervative