Long Noncoding RNA AFAP1-AS1 Promotes Cell Proliferation and Apoptosis of Gastric Cancer Cells via PTEN/p-AKT Pathway.

<bold>Background: </bold>Long noncoding RNA (lncRNA) plays critical roles in both tumor-suppressive and oncogenic pathways in the pathological development and prognosis of cancers.<bold>Aims: </bold>This study aimed to explore the expression of lncRNA AFAP1-AS1 and its function in gastric cancer (GC).<bold>Methods: </bold>The expression of AFAP1-AS1 was detected in GC tissues and GC cells by quantitative real-time reverse-transcription PCR. A small interfering RNA (siRNA) that targeted AFAP1-AS1 was transfected into cells to inhibit the expression of AFAP1-AS1. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and colony formation assay were performed to examine the cell proliferation of SGC7901 cell transfected with si-AFAP1-AS1. Cell apoptosis was detected by flow cytometry. The protein level of cleaved PARP, Caspase 3, Caspase 9, Caspase 8, Bcl-2, Bax, p-AKT, total-AKT, and PTEN were detected by Western blot.<bold>Results: </bold>AFAP1-AS1 was up-regulated in GC tissues and GC cells. AFAP1-AS1 knockdown suppressed cell viability of SGC7901 transfected with si-AFAP1-AS1. The number of apoptotic SGC7901 cell transfected with si-AFAP1-AS1 was increased by 3.4-fold comparing to that of control. The protein level of cleaved PARP, Caspase 3, and Caspase 9 were increased in SGC7901 transfected with si-AFAP1-AS1, as well as the expression of Bax. The protein level of Bcl-2 was decreased. AFAP1-AS1 knockdown decreased the protein level of p-AKT and increased the expression of PTEN in SGC7901 cells.<bold>Conclusions: </bold>AFAP1-AS1 was up-regulated in GC cells and regulated the gastric cancer cell proliferation and apoptosis via PTEN/p-AKT pathway. [ABSTRACT FROM AUTHOR]