Abstract

Long non-coding RNA (lncRNA) actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) has been revealed to be associated with certain types of cancer. However, whether the lncRNA AFAP1-AS1 is involved in the development and progression of gastric cancer (GC) remains unknown. The present study investigated the clinical significance and biological functions of AFAP1-AS1 in GC. The expression levels of lncRNA AFAP1-AS1 in 52 patients with GC, and in 1 normal gastric mucosal cell line and 3 GC cell lines, were evaluated by reverse transcription quantitative polymerase chain reaction analysis. Small interfering RNAs were used to suppress AFAP1-AS1 expression in GC cell lines. The results indicated that AFAP1-AS1 expression levels were significantly increased in GC tissues and cell lines compared with the corresponding noncancerous tissues and normal gastric cells. In addition, the patients with GC with increased AFAP1-AS1 expression exhibited an advanced clinical stage and an association with the occurrence of lymph node metastasis compared with those with decreased AFAP1-AS1 expression. In vitro assays demonstrated that knockdown of AFAP1-AS1 decreased levels of cell proliferation and migration. In addition, the results of flow cytometry demonstrated that knockdown of AFAP1-AS1 caused cell cycle arrest. In conclusion, AFAP1-AS1 is a novel molecule involved in GC progression, which may be a potential prognostic biomarker and target for therapeutic intervention.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.