Abstract 5580: Determining the effects of serine-arginine protein kinases inhibition on splicing factors and long non-coding ribonucleic acids regulation in cervical cancer cells

Abstract Cervical cancer (CCa) remains a significant global health challenge, with high morbidity and mortality rates, particularly in developing countries. The pathogenesis of CCa is largely driven by persistent infection with high-risk strains of Human Papillomavirus (HPV). Serine-arginine protein kinases are a family of cell cycle-regulated kinases that phosphorylate the serine/arginine (SR) domain-containing proteins in the nuclear patches to intervene with pre-mRNA splicing, signals splicing controls in response to extracellular stimuli and contributes to tumorigenesis. It has been reported in recent studies that the dysregulation of splicing factors and lncRNAs affects the progression of CCa. The involvement of SRPKs with lncRNAs regulation remains unelucidated in CCa. This study aimed to investigate the association of lncRNAs and SRPKs inhibition by SRPIN340 in CCa cells SiHa and C33A. Alamar blue cell viability assay, 84 lncRNA gene panel, bioinformatics analysis and RT-qPCR were used to achieve the aim of the study. SRPIN340 showed no cytotoxicity to CCa. Differential lncRNA gene expression, favoring CCa progressing was observed and these results were verified by increased expressions of MALAT1 and TUG1. The association between splicing factors and lncRNAs is complex, as influence of these 2 parities may be bi-directional. Understating this relationship may unlock diagnostic, prognostic and therapeutic targets in CCa. Citation Format: Lydia Mphahlele, Zodwa Dlamini, Rahaba Makgotso Marima. Determining the effects of serine-arginine protein kinases inhibition on splicing factors and long non-coding ribonucleic acids regulation in cervical cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 5580.