QKI-Regulated Alternative Splicing Events in Cervical Cancer: Pivotal Mechanism and Potential Therapeutic Strategy

QKI is a vital regulator in RNA splicing and maturation, but its role in cervical cancer (CC) is little known. In this study, we found that QKI is decreased in human CC, and overexpression of QKI inhibits HeLa cell proliferation and promotes the apoptosis of cancer cells. We identified hundreds of endogenous QKI-regulated alternative splicing events (ASEs) and differentially expressed genes (DEGs) in QKI-overexpressed HeLa cells by RNA-seq and selectively validated their expression by quantitative reverse-transcription polymerase chain reaction. The gene ontology and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis showed that QKI-regulated ASEs and DEGs were closely related to cancer, apoptosis, and transcriptional regulatory functions. In short, QKI may affect the occurrence and development of CC by regulating gene expression through AS.

Automated summary

QKI is found to be reduced in human cervical cancer, and its overexpression inhibits cell proliferation and promotes apoptosis. Through RNA-seq and qRT-PCR, hundreds of QKI-regulated alternative splicing events and differentially expressed genes were identified, closely related to cancer, apoptosis, and transcriptional regulation functions. In conclusion, QKI may impact the occurrence and development of cervical cancer by regulating gene expression through alternative splicing.