Knockdown of Long Noncoding RNA-Encoding Gene RP11-10C24.1 Suppresses Pancreatic Cancer Cell Growth In Vitro and In Vivo.

High expression of long noncoding RNA-encoding gene RP11-10C24.1 is associated with poor survival of patients with pancreatic cancer. This study aimed to investigate the role of RP11-10C24.1 in pancreatic cancer cell growth. The RNA sequencing and survival data of 177 patients with pancreatic cancer were acquired from TCGA to screen survival-associated lncRNAs. RNA BaseScope was used to retrospectively examine RP11-10C24.1 expression in 54 pairs of pancreatic cancer and paracancer samples of real-world patients. Fluorescence in situ hybridization (FISH) was conducted to localize RP11-10C24.1 transcripts in pancreatic cancer cells. Knockdown of RP11-10C24.1 was performed to investigate the role of RP11-10C24.1 in the behavior of pancreatic cancer cells in vitro and in vivo. Western blot analysis was carried out to identify the functional targets downstream of RP11-10C24.1. High expression of RP11-10C24.1 was associated with poor survival of the TCGA cohort. RP11-10C24.1 expression was significantly increased in pancreatic cancer tissue compared with that in paracancer tissue. FISH analysis demonstrated that RP11-10C24.1 transcript was localized in the cytoplasm of pancreatic cancer cells. In PANC-1, SW1990, and AsPC-1 cells, knockdown of RP11-10C24.1 inhibited cell proliferation, migration, and invasion while promoting cell apoptosis. Knockdown of RP11-10C24.1 suppressed the growth of AsPC-1 tumor xenografts in mice. Furthermore, knockdown of RP11-10C24.1 attenuated protein expression of multiple cancer-associated genes, including fibronectin 1 (FN1), in PANC-1 cells. Importantly, overexpression of FN1 effectively reversed the suppressive effect of RP11-10C24.1 silencing on pancreatic cell proliferation and invasion. In conclusion, knockdown of RP11-10C24.1 inhibits pancreatic cancer cell growth through downregulating FN1 expression.