Long non-coding RNA CERS6-AS1 facilitates the oncogenicity of pancreatic ductal adenocarcinoma by regulating the microRNA-15a-5p/FGFR1 axis
Zhennan Yun, Fanqi Meng, Shiquan Li, Ping Zhang
Abstract
Mechanistically, CERS6-AS1 could competitively bind to microRNA-15a-5p (miR-15a-5p) and effectively work as a molecular sponge in PDAC cells, resulting in the upregulation of fibroblast growth factor receptor 1 (FGFR1), a direct target of miR-15a-5p. Rescue experiments revealed that miR-15a-5p downregulation or FGFR1 restoration rescued the effects of CERS6-AS1 knockdown on the behaviors of PDAC cells. In conclusion, CERS6-AS1 promoted the oncogenicity of PDAC by serving as a competing endogenous RNA to sequester miR-15a-5p and increase FGFR1 expression, which highlights the potential of the CERS6-AS1/miR-15a-5p/FGFR1 pathway as an effective target for cancer therapy.
Topics & Concepts
Pancreatic ductal adenocarcinomamicroRNAFibroblast growth factor receptor 1Long non-coding RNACancer researchRNABiologyPancreatic cancerInternal medicineMedicineGeneCancerFibroblast growth factorGeneticsReceptorCancer-related molecular mechanisms researchMicroRNA in disease regulationCircular RNAs in diseases