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.