Furthermore, ectopic SCIRT expression upregulated SFPQ and activated the PI3K/Akt pathway following CPT treatment, suggesting an unexpected role of SCIRT in facilitating SFPQ-mediated DSB repair. In brief, our findings highlight the oncogenic role of SCIRT in NSCLC by binding SFPQ and activating PI3K/Akt signaling, presenting a promising therapeutic target for personalized NSCLC treatment.
Knockdown/overexpressing SCIRT affected CC proliferative/invasive properties. Hence, lncRNA SCIRT is a promising drug-target and a new biological diagnostic molecule for CC patients.