Abstract Objective Gallbladder carcinoma (GBC) is a common malignancy of the biliary tract that, with late diagnosis, is often fatal. A better understanding of the underlying molecular mechanisms may facilitate… Click to show full abstract
Abstract Objective Gallbladder carcinoma (GBC) is a common malignancy of the biliary tract that, with late diagnosis, is often fatal. A better understanding of the underlying molecular mechanisms may facilitate targeted therapy for GBC. Therefore, this study aimed to investigate whether long non-coding RNA AFAP1-AS1 regulates GBC cell proliferation and apoptosis through hsa-miR-15a-5p. Methods SGC-996 and NOZ cell lines were transfected with an hsa-mR-15a-5p inhibitor or si-AFAP1-AS1, and GBC cell proliferation and apoptosis were measured. The expression levels of AFAP1-AS1, hsa-miR-15a-5p, apoptosis-related proteins, and bcl-2 were assessed. The dual-luciferase reporter assay was used to determine the binding between AFAP1-AS1 and hsa-miR-15a-5p or between hsa-miR-15a-5p and bcl-1. Results In SGC-996 and NOZ cells, AFAP1-AS1 was significantly expressed and hsa-miR-15a-5p was modestly expressed. Transfection of the hsa-miR-15a-5p inhibitor elevated proliferation of SGC-996 and NOZ cells and decreased apoptosis, whereas transfection of si-AFAP1-AS1 reduced the proliferation rate and increased apoptosis. In addition, AFAP1-AS1 bound hsa-miR-15a-5p and hsa-miR-15a-5p targeted bcl-2. Increased bcl-2 expression was observed in the GBC cells. AFAP1-AS1 may regulate GBC cell proliferation and apoptosis via has-miR-15a-5p to mediate bcl-2 expression. Conclusion The AFAP1-AS1/hsa-miR-15a-5p/bcl-2 axis regulates GBC cell proliferation and apoptosis, providing potential guidance for the clinical treatment of GBC.
               
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